Weiming Yan, Yan Sun, Yutong Wang, Wangjiao Liang, Yuxin Xia, Weihua Yan, Meizhu Chen, Tao Chen, Dongliang Li
{"title":"The impacts of resveratrol on the retinal degeneration in a rat model of retinitis pigmentosa induced by alkylation: an in-vivo study.","authors":"Weiming Yan, Yan Sun, Yutong Wang, Wangjiao Liang, Yuxin Xia, Weihua Yan, Meizhu Chen, Tao Chen, Dongliang Li","doi":"10.1080/19768354.2023.2226695","DOIUrl":"https://doi.org/10.1080/19768354.2023.2226695","url":null,"abstract":"<p><p>Upregulation of Sirtuin Type 1 (SIRT1), a nicotinamide adeninedinucleotide (NAD<sup>+</sup>)-dependent deacetylase, has been proved to protect against ample ocular diseases, while its effect on retinitis pigmentosa (RP) has not been illustrated. The study was aimed to explore the impacts of resveratrol (RSV), a SIRT1 activator, on the photoreceptor degeneration in a rat model of RP induced by N-methyl-N-nitrosourea (MNU), an alkylation. The rats were induced RP phenotypes via the intraperitoneal injection of MNU. The electroretinogram was conducted and revealed that RSV could not prevent the decline of retinal function in the RP rats. The optical coherence tomography (OCT) and the retinal histological examination were performed and showed that the reduced thickness of the outer nuclear layer (ONL) was not preserved by RSV intervention. The immunostaining technique was applied. Afther the MNU administration, the number of the apoptotic photoreceptors in the ONL throughout the retinasand the number of microglia cells present among the outer part throughout the retinas were not significantly reduced by RSV. Western blotting was also performed. The data showed that the level of SIRT1 protein was decreased after MNU administration, while RSV was not able to obviously alleviate the downregulation. Our data together indicated that RSV was not able to rescue the photoreceptor degeneration in the MNU-induced RP rats, which might be due to the MNU-induced consumption of the NAD<sup>+</sup>.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"138-148"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10304456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9741454","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}
{"title":"Association of overexpressed carboxyl-terminal amyloid precursor protein in brains with altered glucose metabolism and liver toxicity.","authors":"Sungguan Hong, Seungwoo Hong, Sung Hoon Lee","doi":"10.1080/19768354.2023.2197761","DOIUrl":"https://doi.org/10.1080/19768354.2023.2197761","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most prevalent neurodegenerative disease. The deposition of amyloid plaques mainly composed of amyloid beta (Aβ) is observed in brain regions in AD patients. AD presents with similar pathophysiology to that of metabolic syndrome, including glucose and insulin resistance. In addition, epidemiological studies indicate diabetes, impaired glucose metabolism, and obesity increase the prevalence of AD. The liver is considered a key organ in the reciprocal relationship between AD and metabolic syndrome and is the major organ for the clearance of Aβ in the periphery. Furthermore, liver dysfunction aggravates Aβ-induced pathophysiology. Aβ is produced in the brain and peripheral tissues and penetrates the blood-brain barrier. However, <i>in vivo</i> evidence showing the effect of Aβ on the crosstalk between the brain and liver has not been reported yet. In the present study, we investigated the toxicity of brain-derived Aβ on glucose metabolism and the liver using transgenic mice overexpressing the carboxyl-terminal of amyloid precursor protein in the brain. The transgenic mice were overweight, which was associated with impaired glucose metabolism and insulin resistance, but not due to increased food intake. In addition, transgenic mice had enlarged livers and reduced gene expressions associated with glucose and lipid metabolism. Thus, overexpressed amyloid precursor protein in the brain may promote being overweight and glucose resistance, possibly through liver toxicity.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"103-111"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10075522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9271799","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}
Soohyun Kim, Sojung Sun, Minbi Kim, Jinah Ha, Eunji Seok, Hyunwon Yang
{"title":"NUCB2/nesfatin-1 suppresses the acrosome reaction in sperm within the mouse epididymis.","authors":"Soohyun Kim, Sojung Sun, Minbi Kim, Jinah Ha, Eunji Seok, Hyunwon Yang","doi":"10.1080/19768354.2023.2212741","DOIUrl":"https://doi.org/10.1080/19768354.2023.2212741","url":null,"abstract":"<p><p>Nesfatin-1, a polypeptide hormone derived from the nucleobindin 2 (NUCB2) precursor protein, is known to regulate appetite and energy metabolism. Recent studies have also shown that NUCB2/nesfatin-1 is expressed in the reproductive organs of mice. However, the expression and potential role of NUCB2/nesfatin-1 in the mouse epididymis remain unclear. Therefore, we investigated the expression of NUCB2/nesfatin-1 in the mouse epididymis and its potential function. NUCB2/nesfatin-1 was detected in the epididymis by qRT-PCR and western blotting, and high expression levels were observed in epididymal epithelial cells by immunohistochemical staining. Pregnant mare's serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) injections significantly increased NUCB2/nesfatin-1 expression in the epididymis. After castration, NUCB2/nesfatin-1 expression in the epididymis decreased, but was significantly increased by testosterone injection. Nesfatin-1-binding sites were found in the middle piece of testicular sperm, but were scarcely detected in the sperm head. By contrast, nesfatin-1 binding sites were identified on the sperm head within the epididymis. Furthermore, nesfatin-1 treatment inhibited the acrosome reaction in epididymal sperm. These results suggest that the nesfatin-1 protein produced in the epididymis binds to nesfatin-1 binding sites on the sperm head and plays a role in suppressing the acrosome reaction before ejaculation.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"120-128"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/21/b8/TACS_27_2212741.PMC10184593.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9541323","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}
Soomin Lim, Hye Jung Ihn, Ju Ang Kim, Jong-Sup Bae, Jung-Eun Kim, Yong Chul Bae, Hong-In Shin, Tae Hoon Kim, Eui Kyun Park
{"title":"Suppressive effects of (-)-tubaic acid on RANKL-induced osteoclast differentiation and bone resorption.","authors":"Soomin Lim, Hye Jung Ihn, Ju Ang Kim, Jong-Sup Bae, Jung-Eun Kim, Yong Chul Bae, Hong-In Shin, Tae Hoon Kim, Eui Kyun Park","doi":"10.1080/19768354.2023.2166107","DOIUrl":"https://doi.org/10.1080/19768354.2023.2166107","url":null,"abstract":"<p><p>Regulation of osteoclastogenesis and bone-resorbing activity can be an efficacious strategy for treating bone loss diseases because excessive osteoclastic bone resorption leads to the development of such diseases. Here, we investigated the role of (-)-tubaic acid, a thermal degradation product of rotenone, in osteoclast formation and function in an attempt to identify alternative natural compounds. (-)-Tubaic acid significantly inhibited receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclast differentiation at both the early and late stages, suggesting that (-)-tubaic acid affects the commitment and differentiation of osteoclast progenitors as well as the cell-cell fusion of mononuclear osteoclasts. (-)-Tubaic acid attenuated the activation of extracellular signal-regulated kinase (ERK) and expression of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and its target genes in response to RANKL. Furthermore, a pit-formation assay revealed that (-)-tubaic acid significantly impaired the bone-resorbing activity of osteoclasts. Our results demonstrated that (-)-tubaic acid exhibits anti-osteoclastogenic and anti-resorptive effects, indicating its therapeutic potential in the management of osteoclast-related bone diseases.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9873279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10681406","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}
{"title":"A genomic estimated breeding value-assisted reduction method of single nucleotide polymorphism sets: a novel approach for determining the cutoff thresholds in genome-wide association studies and best linear unbiased prediction.","authors":"Young-Sup Lee, Jae-Don Oh, Jun-Yeong Lee, Donghyun Shin","doi":"10.1080/19768354.2023.2250841","DOIUrl":"https://doi.org/10.1080/19768354.2023.2250841","url":null,"abstract":"<p><p>Traditionally, the <i>p</i>-value is the criterion for the cutoff threshold to determine significant markers in genome-wide association studies (GWASs). Choosing the best subset of markers for the best linear unbiased prediction (BLUP) for improved prediction ability (PA) has become an interesting issue. However, when dealing with many traits having the same marker information, the <i>p</i>-values' themselves cannot be used as an obvious solution for having a confidence in GWAS and BLUP. We thus suggest a genomic estimated breeding value-assisted reduction method of the single nucleotide polymorphism (SNP) set (GARS) to address these difficulties. GARS is a BLUP-based SNP set decision presentation. The samples were Landrace pigs and the traits used were back fat thickness (BF) and daily weight gain (DWG). The prediction abilities (PAs) for BF and DWG for the entire SNP set were 0.8 and 0.8, respectively. By using the correlation between genomic estimated breeding values (GEBVs) and phenotypic values, selecting the cutoff threshold in GWAS and the best SNP subsets in BLUP was plausible as defined by GARS method. 6,000 SNPs in BF and 4,000 SNPs in DWG were considered as adequate thresholds. Gene Ontology (GO) analysis using the GARS results of the BF indicated neuron projection development as the notable GO term, whereas for the DWG, the main GO terms were nervous system development and cell adhesion.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"180-186"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10478620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10199819","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}
{"title":"The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder.","authors":"Ji Young Kim, Wanil Kim, Kyung-Ha Lee","doi":"10.1080/19768354.2023.2180535","DOIUrl":"https://doi.org/10.1080/19768354.2023.2180535","url":null,"abstract":"<p><p>Circadian rhythm regulates physiological cycles of awareness and sleepiness. Melatonin production is primarily regulated by circadian regulation of gene expression and is involved in sleep homeostasis. If the circadian rhythm is abnormal, sleep disorders, such as insomnia and several other diseases, can occur. The term 'autism spectrum disorder (ASD)' is used to characterize people who exhibit a certain set of repetitive behaviors, severely constrained interests, social deficits, and/or sensory behaviors that start very early in life. Because many patients with ASD suffer from sleep disorders, sleep disorders and melatonin dysregulation are attracting attention for their potential roles in ASD. ASD is caused by abnormalities during the neurodevelopmental processes owing to various genetic or environmental factors. Recently, the role of microRNAs (miRNAs) in circadian rhythm and ASD have gained attraction. We hypothesized that the relationship between circadian rhythm and ASD could be explained by miRNAs that can regulate or be regulated by either or both. In this study, we introduced a possible molecular link between circadian rhythm and ASD. We performed a thorough literature review to understand their complexity.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"38-52"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9970207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9238265","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}
Yan Sun, Seung-Min Lee, Bon-Jin Ku, Myung-Jin Moon
{"title":"Fine structural aspects on the web glue production in the golden orb-web spider <i>Trichonephila clavata</i>.","authors":"Yan Sun, Seung-Min Lee, Bon-Jin Ku, Myung-Jin Moon","doi":"10.1080/19768354.2023.2168753","DOIUrl":"https://doi.org/10.1080/19768354.2023.2168753","url":null,"abstract":"<p><p>The water-soluble glue substance of the capture threads in <i>Trichonephila clavata</i> is solely produced from two pairs of aggregate silk glands. During the web glue production, secretory vesicles were synthesized via the extensive rough endoplasmic reticulum of epithelial cells. Unlike the clearly described fibrous web production in spiders, the process of aqueous web glue production appears to involve either a condensing or a packaging step by the Golgi complex. In particular, the fine structure of secretory vesicles varies from cell to cell and may represent the secretory cycle. The electron-dense multivesicular bodies were clearly visible as discrete droplets, and the mature secretory product in the glandular epithelium appeared as a spherical vacuole grown by fusion with surrounding small vesicles. Our fine structural observation reveals that the secretion occurs when the release of secreted material involves the loss of part of the cytoplasm. The bleb along the luminal surface of the secretory cells and membrane-bound extracellular vesicles which pinched off from the cell suggests that the secretory product is released by the mechanism of apocrine secretion.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"10-18"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9888464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10700121","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}
{"title":"Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases.","authors":"Junhee Kwon, Jihyun Kim, Keun Il Kim","doi":"10.1080/19768354.2023.2181217","DOIUrl":"https://doi.org/10.1080/19768354.2023.2181217","url":null,"abstract":"<p><p>Cells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"29-37"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9970256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10812289","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}
{"title":"Emerging roles of polyunsaturated fatty acid synthesis pathway in colorectal cancer.","authors":"Young-Ah Moon","doi":"10.1080/19768354.2023.2189933","DOIUrl":"https://doi.org/10.1080/19768354.2023.2189933","url":null,"abstract":"<p><p>The development of colorectal cancer typically involves the accumulated influences of genetic alterations, medical issues, lifestyle, and diet. Dietary fatty acids appear to affect the tumorigenesis and progression of colorectal cancer. Despite conflicting results, the current consensus on the effects of very long-chain polyunsaturated fatty acids on colorectal cancer is that low levels of eicosapentaenoic acid and docosahexaenoic acid, and high levels of arachidonic acid are associated with an increased risk of colorectal cancer. Altered levels of arachidonic acid in membrane phospholipids can change the levels of prostaglandin E<sub>2</sub>, which affect the biological activities of cancer cells in multiple stages. Arachidonic acid and other very long-chain polyunsaturated fatty acids can affect tumorigenesis in prostaglandin E<sub>2</sub>-independent manners as well, including stabilization of β-catenine, ferroptosis, ROS generation, regulation of transcription factors, and de novo lipogenesis. Recent studies have revealed an association between the activities of enzymes synthesizing very long-chain polyunsaturated fatty acids and tumorigenesis and cancer progression, although the mechanisms are still unknown. In this study, PUFA effects on tumorigenesis, the endogenous very long-chain polyunsaturated fatty acid synthesis pathway, metabolites of arachidonic acid and their effects on tumorigenesis and progression of CRC, and current knowledge that supports the association of the enzymes involved in the polyunsaturated fatty acid synthesis pathway with colorectal cancer tumorigenesis and progression are reviewed.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"61-71"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9561614","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}
{"title":"Chloromethylisothiazolinone induces ER stress-induced stress granule formation in human keratinocytes.","authors":"Da-Min Jung, Kee K Kim, Eun-Mi Kim","doi":"10.1080/19768354.2023.2250852","DOIUrl":"https://doi.org/10.1080/19768354.2023.2250852","url":null,"abstract":"<p><p>Chloromethylisothiazolinone (CMIT), a humidifier disinfectant, is known to be toxic to the respiratory system. While the toxic effect of CMIT on the lungs has been widely investigated, its effect on the skin is well unknown. In this study, we examined stress granule (SG) formation to investigate the cytotoxic effects of CMIT on human keratinocytes. We assessed the viability of the cells following CMIT exposure and performed immunofluorescence microscopy and immunoblot analyses to determine SG formation and downstream pathways. The IC<sub>50</sub> values in human keratinocyte HaCaT cells after CMIT exposure for 1 and 24 h were 11 and 8 μg/mL, respectively, showing no significant difference. As determined using immunofluorescence microscopy, SG formation was effectively induced after CMIT exposure. Moreover, the phosphorylation of eukaryotic initiation factor-2α (eIF2α), a translation initiation factor, and protein kinase R-like endoplasmic reticulum (ER) kinase, which plays a role in the ER stress-mediated eIF2α phosphorylation, was confirmed by CMIT exposure. These results suggest that exposure to CMIT can have detrimental effects on the skin, even briefly, by inducing SG formation through ER stress in keratinocytes.</p>","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"27 1","pages":"171-179"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10448836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10197251","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}