IF 5.1 2区生物学

Cells Pub Date : 2025-03-06 DOI: 10.3390/cells14050384

Mengyang Xu, Ethan Y Zhou, Haifei Shi

{"title":"Tryptophan and Its Metabolite Serotonin Impact Metabolic and Mental Disorders via the Brain-Gut-Microbiome Axis: A Focus on Sex Differences.","authors":"Mengyang Xu, Ethan Y Zhou, Haifei Shi","doi":"10.3390/cells14050384","DOIUrl":"10.3390/cells14050384","url":null,"abstract":"The crisis of metabolic and mental disorders continues to escalate worldwide. A growing body of research highlights the influence of tryptophan and its metabolites, such as serotonin, beyond their traditional roles in neural signaling. Serotonin acts as a key neurotransmitter within the brain-gut-microbiome axis, a critical bidirectional communication network affecting both metabolism and behavior. Emerging evidence suggests that the gut microbiome regulates brain function and behavior, particularly through microbial influences on tryptophan metabolism and the serotonergic system, both of which are essential for normal functioning. Additionally, sex differences exist in multiple aspects of serotonin-mediated modulation within the brain-gut-microbiome axis, affecting feeding and affective behaviors. This review summarizes the current knowledge from human and animal studies on the influence of tryptophan and its metabolite serotonin on metabolic and behavioral regulation involving the brain and gut microbiome, with a focus on sex differences and the role of sex hormones. We speculate that gut-derived tryptophan and serotonin play essential roles in the pathophysiology that modifies neural circuits, potentially contributing to eating and affective disorders. We propose the gut microbiome as an appealing therapeutic target for metabolic and affective disorders, emphasizing the importance of understanding sex differences in metabolic and behavioral regulation influenced by the brain-gut-microbiome axis. The therapeutic targeting of the gut microbiota and its metabolites may offer a viable strategy for treating serotonin-related disorders, such as eating and affective disorders, with potential differences in treatment efficacy between men and women. This review would promote research on sex differences in metabolic and behavioral regulation impacted by the brain-gut-microbiome axis.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11899299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Selective Azapeptide CD36 Ligand MPE-298 Regulates oxLDL-LOX-1-Mediated Inflammation and Mitochondrial Oxidative Stress in Macrophages.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-06 DOI: 10.3390/cells14050385

Mukandila Mulumba, Catherine Le, Emmanuelle Schelsohn, Yoon Namkung, Stéphane A Laporte, Maria Febbraio, Marc J Servant, Sylvain Chemtob, William D Lubell, Sylvie Marleau, Huy Ong

{"title":"Selective Azapeptide CD36 Ligand MPE-298 Regulates oxLDL-LOX-1-Mediated Inflammation and Mitochondrial Oxidative Stress in Macrophages.","authors":"Mukandila Mulumba, Catherine Le, Emmanuelle Schelsohn, Yoon Namkung, Stéphane A Laporte, Maria Febbraio, Marc J Servant, Sylvain Chemtob, William D Lubell, Sylvie Marleau, Huy Ong","doi":"10.3390/cells14050385","DOIUrl":"10.3390/cells14050385","url":null,"abstract":"Macrophage mitochondrial dysfunction, caused by oxidative stress, has been proposed as an essential event in the progression of chronic inflammation diseases, such as atherosclerosis. The cluster of differentiation-36 (CD36) and lectin-like oxLDL receptor-1 (LOX-1) scavenger receptors mediate macrophage uptake of oxidized low-density lipoprotein (oxLDL), which contributes to mitochondrial dysfunction by sustained production of mitochondrial reactive oxygen species (mtROS), as well as membrane depolarization. In the present study, the antioxidant mechanisms of action of the selective synthetic azapeptide CD36 ligand MPE-298 have been revealed. After binding to CD36, MPE-298 was rapidly internalized by and simultaneously induced CD36 endocytosis through activation of the Lyn and Syk (spleen) tyrosine kinases. Within this internalized complex, MPE-298 inhibited oxLDL/LOX-1-induced chemokine ligand 2 (CCL2) secretion, abolished the production of mtROS, and prevented mitochondrial membrane potential depolarization in macrophages. This occurred through the inhibition of the multiple-component enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) by oxLDL-activated LOX-1, which was further supported by the reduced recruitment of the p47phox subunit and small GTPase (Rac) 1/2/3 into the plasma membrane. A new mechanism for alleviating oxLDL-induced oxidative stress and inflammation in macrophages is highlighted using the CD36 ligand MPE-298.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Beneficial Role of the Thyroid Hormone Receptor Beta 2 (thrb2) in Facilitating the First Feeding and Subsequent Growth in Medaka as Fish Larval Model.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-06 DOI: 10.3390/cells14050386

Jiaqi Wu, Ke Lu, Ruipeng Xie, Chenyuan Zhu, Qiyao Luo, Xu-Fang Liang

{"title":"The Beneficial Role of the Thyroid Hormone Receptor Beta 2 (thrb2) in Facilitating the First Feeding and Subsequent Growth in Medaka as Fish Larval Model.","authors":"Jiaqi Wu, Ke Lu, Ruipeng Xie, Chenyuan Zhu, Qiyao Luo, Xu-Fang Liang","doi":"10.3390/cells14050386","DOIUrl":"10.3390/cells14050386","url":null,"abstract":"During the early growth stages of fish larvae, there are significant challenges to their viability, so improving their visual environment is essential to promoting their growth and survival. Following the successful knockout of thyroid hormone receptor beta 2 (thrb2) using Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 technology, there was an increase in the expression of UV opsin (short-wave-sensitive 1, sws1), while the expression of other cone opsins was significantly decreased. Further analysis of the retinal structure demonstrated that the thrb2 knockout resulted in an increased lens thickness and a decreased thickness of the ganglion cell layer (GCL), outer plexiform layer (OPL), and outer nuclear layer (ONL) in the retina. The slowing down of swimming speed under light conditions in thrb2-/- may be related to the decreased expression of phototransduction-related genes such as G protein-coupled receptor kinase 7a (grk7a), G protein-coupled receptor kinase 7b (grk7b), and phosphodiesterase 6c (pde6c). Notably, thrb2-/- larvae exhibited a significant increase in the amount and proportion of first feeding, and their growth rate significantly exceeded that of wild-type controls during the week after feeding. This observation suggests that although the development of the retina may be somewhat affected, thrb2-/- larvae show positive changes in feeding behaviour and growth rate, which may be related to their enhanced ability to adapt to their environment. These results provide novel insights into the function of the thrb2 gene in the visual system and behaviour and may have implications in areas such as fish farming and genetic improvement.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HOTAIR Participation in Glycolysis and Glutaminolysis Through Lactate and Glutamate Production in Colorectal Cancer.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-06 DOI: 10.3390/cells14050388

Laura Cecilia Flores-García, Verónica García-Castillo, Eduardo Pérez-Toledo, Samuel Trujano-Camacho, Oliver Millán-Catalán, Eloy Andrés Pérez-Yepez, Jossimar Coronel-Hernández, Mauricio Rodríguez-Dorantes, Nadia Jacobo-Herrera, Carlos Pérez-Plasencia

{"title":"HOTAIR Participation in Glycolysis and Glutaminolysis Through Lactate and Glutamate Production in Colorectal Cancer.","authors":"Laura Cecilia Flores-García, Verónica García-Castillo, Eduardo Pérez-Toledo, Samuel Trujano-Camacho, Oliver Millán-Catalán, Eloy Andrés Pérez-Yepez, Jossimar Coronel-Hernández, Mauricio Rodríguez-Dorantes, Nadia Jacobo-Herrera, Carlos Pérez-Plasencia","doi":"10.3390/cells14050388","DOIUrl":"10.3390/cells14050388","url":null,"abstract":"Metabolic reprogramming plays a crucial role in cancer biology and the mechanisms underlying its regulation represent a promising study area. In this regard, the discovery of non-coding RNAs opened a new regulatory landscape, which is in the early stages of investigation. Using a differential expression model of HOTAIR, we evaluated the expression level of metabolic enzymes, as well as the metabolites produced by glycolysis and glutaminolysis. Our results demonstrated the regulatory effect of HOTAIR on the expression of glycolysis and glutaminolysis enzymes in colorectal cancer cells. Specifically, through the overexpression and inhibition of HOTAIR, we determined its influence on the expression of the enzymes PFKFB4, PGK1, LDHA, SLC1A5, GLUD1, and GOT1, which had a direct impact on lactate and glutamate production. These findings indicate that HOTAIR plays a significant role in producing \"oncometabolites\" essential to maintaining the bioenergetics and biomass necessary for tumor cell survival by regulating glycolysis and glutaminolysis.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The LSmAD Domain of Ataxin-2 Modulates the Structure and RNA Binding of Its Preceding LSm Domain.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-06 DOI: 10.3390/cells14050383

Shengping Zhang, Yunlong Zhang, Ting Chen, Hong-Yu Hu, Changrui Lu

{"title":"The LSmAD Domain of Ataxin-2 Modulates the Structure and RNA Binding of Its Preceding LSm Domain.","authors":"Shengping Zhang, Yunlong Zhang, Ting Chen, Hong-Yu Hu, Changrui Lu","doi":"10.3390/cells14050383","DOIUrl":"10.3390/cells14050383","url":null,"abstract":"Ataxin-2 (Atx2), an RNA-binding protein, plays a pivotal role in the regulation of RNA, intracellular metabolism, and translation within the cellular environment. Although both the Sm-like (LSm) and LSm-associated (LSmAD) domains are considered to associated with RNA binding, there is still a lack of experimental evidence supporting their functions. To address this, we designed and constructed several recombinants containing the RNA-binding domain (RBD) of Atx2. By employing biophysical and biochemical techniques, such as EMSA and SHAPE chemical detection, we identified that LSm is responsible for RNA binding, whereas LSmAD alone does not bind RNA. NMR and small-angle X-ray scattering (SAXS) analyses have revealed that the LSmAD domain exhibits limited structural integrity and poor folding capability. The EMSA data confirmed that both LSm and LSm-LSmAD bind RNA, whereas LSmAD alone cannot, suggesting that LSmAD may serve as an auxiliary role to the LSm domain. SHAPE chemical probing further demonstrates that LSm binds to the AU-rich, GU-rich, or CU-rich sequence, but not to the CA-rich sequence. These findings indicate that Atx2 can interact with the U-rich sequences in the 3'-UTR, implicating its role in poly(A) tailing and the regulation of mRNA translation and degradation.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-05 DOI: 10.3390/cells14050378

Francisco Santos, Hashum Sum, Denise Cheuk Lee Yan, Alison C Brewer

{"title":"Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.","authors":"Francisco Santos, Hashum Sum, Denise Cheuk Lee Yan, Alison C Brewer","doi":"10.3390/cells14050378","DOIUrl":"10.3390/cells14050378","url":null,"abstract":"Endothelial dysfunction is the main initiating factor in atherosclerosis. Through mechanotransduction, shear stress regulates endothelial cell function in both homeostatic and diseased states. Accumulating evidence reveals that epigenetic changes play critical roles in the etiology of cardiovascular diseases, including atherosclerosis. The metabolic regulation of epigenetics has emerged as an important factor in the control of gene expression in diseased states, but to the best of our knowledge, this connection remains largely unexplored in endothelial dysfunction and atherosclerosis. In this review, we (1) summarize how shear stress (or flow) regulates endothelial (dys)function; (2) explore the epigenetic alterations that occur in the endothelium in response to disturbed flow; (3) review endothelial cell metabolism under different shear stress conditions; and (4) suggest mechanisms which may link this altered metabolism to the regulation of the endothelial epigenome by modulations in metabolite availability. We believe that metabolic regulation plays an important role in endothelial epigenetic reprogramming and could pave the way for novel metabolism-based therapeutic strategies.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Podocyte A20/TNFAIP3 Controls Glomerulonephritis Severity via the Regulation of Inflammatory Responses and Effects on the Cytoskeleton.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-05 DOI: 10.3390/cells14050381

Paulina Köhler, Andrea Ribeiro, Mohsen Honarpisheh, Ekaterina von Rauchhaupt, Georg Lorenz, Chenyu Li, Lucas Martin, Stefanie Steiger, Maja Lindenmeyer, Christoph Schmaderer, Hans-Joachim Anders, Dana Thomasova, Maciej Lech

{"title":"Podocyte A20/TNFAIP3 Controls Glomerulonephritis Severity via the Regulation of Inflammatory Responses and Effects on the Cytoskeleton.","authors":"Paulina Köhler, Andrea Ribeiro, Mohsen Honarpisheh, Ekaterina von Rauchhaupt, Georg Lorenz, Chenyu Li, Lucas Martin, Stefanie Steiger, Maja Lindenmeyer, Christoph Schmaderer, Hans-Joachim Anders, Dana Thomasova, Maciej Lech","doi":"10.3390/cells14050381","DOIUrl":"10.3390/cells14050381","url":null,"abstract":"A20/Tnfaip3, an early NF-κB response gene and key negative regulator of NF-κB signaling, suppresses proinflammatory responses. Its ubiquitinase and deubiquitinase activities mediate proteasomal degradation within the NF-κB pathway. This study investigated the involvement of A20 signaling alterations in podocytes in the development of kidney injury. The phenotypes of A20Δpodocyte (podocyte-specific knockout of A20) mice were compared with those of control mice at 6 months of age to identify spontaneous changes in kidney function. A20Δpodocyte mice presented elevated serum urea nitrogen and creatinine levels, along with increased accumulation of inflammatory cells-neutrophils and macrophages-within the glomeruli. Additionally, A20Δpodocyte mice displayed significant podocyte loss. Ultrastructural analysis of A20 podocyte-knockout mouse glomeruli revealed hypocellularity of the glomerular tuft, expansion of the extracellular matrix, podocytopenia associated with foot process effacement, karyopyknosis, micronuclei, and podocyte detachment. In addition to podocyte death, we also observed damage to intracapillary endothelial cells with vacuolation of the cytoplasm and condensation of nuclear chromatin. A20 expression downregulation and CRISPR-Cas9 genome editing targeting A20 in a podocyte cell line confirmed these findings in vitro, highlighting the significant contribution of A20 activity in podocytes to glomerular injury pathogenesis. Finally, we analyzed TNFAIP3 transcription levels alongside genes involved in apoptosis, anoikis, NF-κB regulation, and cell attachment in glomerular and tubular compartments of kidney biopsies of patients with various renal diseases.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Histomorphology to Molecular Transition: Exploring the Genomic Landscape of Poorly Differentiated Epithelial Endometrial Cancers.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-05 DOI: 10.3390/cells14050382

Thulo Molefi, Lloyd Mabonga, Rodney Hull, Absalom Mwazha, Motshedisi Sebitloane, Zodwa Dlamini

{"title":"The Histomorphology to Molecular Transition: Exploring the Genomic Landscape of Poorly Differentiated Epithelial Endometrial Cancers.","authors":"Thulo Molefi, Lloyd Mabonga, Rodney Hull, Absalom Mwazha, Motshedisi Sebitloane, Zodwa Dlamini","doi":"10.3390/cells14050382","DOIUrl":"10.3390/cells14050382","url":null,"abstract":"The peremptory need to circumvent challenges associated with poorly differentiated epithelial endometrial cancers (PDEECs), also known as Type II endometrial cancers (ECs), has prompted therapeutic interrogation of the prototypically intractable and most prevalent gynecological malignancy. PDEECs account for most endometrial cancer-related mortalities due to their aggressive nature, late-stage detection, and poor response to standard therapies. PDEECs are characterized by heterogeneous histopathological features and distinct molecular profiles, and they pose significant clinical challenges due to their propensity for rapid progression. Regardless of the complexities around PDEECs, they are still being administered inefficiently in the same manner as clinically indolent and readily curable type-I ECs. Currently, there are no targeted therapies for the treatment of PDEECs. The realization of the need for new treatment options has transformed our understanding of PDEECs by enabling more precise classification based on genomic profiling. The transition from a histopathological to a molecular classification has provided critical insights into the underlying genetic and epigenetic alterations in these malignancies. This review explores the genomic landscape of PDEECs, with a focus on identifying key molecular subtypes and associated genetic mutations that are prevalent in aggressive variants. Here, we discuss how molecular classification correlates with clinical outcomes and can refine diagnostic accuracy, predict patient prognosis, and inform therapeutic strategies. Deciphering the molecular underpinnings of PDEECs has led to advances in precision oncology and protracted therapeutic remissions for patients with these untamable malignancies.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decreased Expression of Aquaporins as a Feature of Tubular Damage in Lupus Nephritis.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-05 DOI: 10.3390/cells14050380

Melchior Maxime, Van Eycken Marie, Nicaise Charles, Duquesne Thomas, Longueville Léa, Collin Amandine, Decaestecker Christine, Salmon Isabelle, Delporte Christine, Soyfoo Muhammad

{"title":"Decreased Expression of Aquaporins as a Feature of Tubular Damage in Lupus Nephritis.","authors":"Melchior Maxime, Van Eycken Marie, Nicaise Charles, Duquesne Thomas, Longueville Léa, Collin Amandine, Decaestecker Christine, Salmon Isabelle, Delporte Christine, Soyfoo Muhammad","doi":"10.3390/cells14050380","DOIUrl":"10.3390/cells14050380","url":null,"abstract":"Background: Tubulointerstitial hypoxia is a key factor for lupus nephritis progression to end-stage renal disease. Numerous aquaporins (AQPs) are expressed by renal tubules and are essential for their proper functioning. The aim of this study is to characterize the tubular expression of AQP1, AQP2 and AQP3, which could provide a better understanding of tubulointerstitial stress during lupus nephritis. Methods: This retrospective monocentric study was conducted at Erasme-HUB Hospital. We included 37 lupus nephritis samples and 9 healthy samples collected between 2000 and 2020, obtained from the pathology department. Immunohistochemistry was performed to target AQP1, AQP2 and AQP3 and followed by digital analysis. Results: No difference in AQP1, AQP2 and AQP3 staining location was found between healthy and lupus nephritis samples. However, we observed significant differences between these two groups, with a decrease in AQP1 expression in the renal cortex and in AQP3 expression in the cortex and medulla. In the subgroup of proliferative glomerulonephritis (class III/IV), this decrease in AQPs expression was more pronounced, particularly for AQP3. In addition, within this subgroup, we detected lower AQP2 expression in patients with higher interstitial inflammation score and lower AQP3 expression when higher interstitial fibrosis and tubular atrophy were present. Conclusions: We identified significant differences in the expression of aquaporins 1, 2, and 3 in patients with lupus nephritis. These findings strongly suggest that decreased AQP expression could serve as an indicator of tubular injury. Further research is warranted to evaluate AQP1, AQP2, and AQP3 as prognostic markers in both urinary and histological assessments of lupus nephritis.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11899336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-34b Regulates Muscle Growth and Development by Targeting SYISL.

IF 5.1 2区生物学

Cells Pub Date : 2025-03-05 DOI: 10.3390/cells14050379

Yuting Wu, Xiao Liu, Yonghui Fan, Hao Zuo, Xiaoyu Niu, Bo Zuo, Zaiyan Xu

{"title":"MiR-34b Regulates Muscle Growth and Development by Targeting SYISL.","authors":"Yuting Wu, Xiao Liu, Yonghui Fan, Hao Zuo, Xiaoyu Niu, Bo Zuo, Zaiyan Xu","doi":"10.3390/cells14050379","DOIUrl":"10.3390/cells14050379","url":null,"abstract":"Non-coding genes, such as microRNA and lncRNA, which have been widely studied, play an important role in the regulatory network of skeletal muscle development. However, the functions and mechanisms of most non-coding RNAs in skeletal muscle regulatory networks are unclear. This study investigated the function and mechanism of miR-34b in muscle growth and development. MiR-34b overexpression and interference tests were performed in C2C12 myoblasts and animal models. It was demonstrated that miR-34b significantly promoted mouse muscle growth and development in vivo, while miR-34b inhibited myoblast proliferation and promoted myoblast differentiation in vitro. Bioinformatics prediction using TargetScan for miRNA target identification and Bibiserv2 for potential miRNA-gene interaction analysis revealed a miR-34b binding site in the SYlSL sequence. The molecular mechanism of miR-34b regulating muscle growth and development was studied by co-transfection experiment, luciferase reporter gene detection, RNA immunoprecipitation, and RNA pull-down. MiR-34b can directly bind to SYISL and AGO2 proteins and regulate the expression of SYISL target genes p21 and MyoG by targeting SYISL, thereby regulating muscle growth and development. This study highlights that, as a novel regulator of myogenesis, miR-34b regulates muscle growth and development by targeting SYISL.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 5","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11898696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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