{"title":"High glucose inhibits neural differentiation by excessive autophagy <em>via</em> peroxisome proliferator-activated receptor gamma.","authors":"Yin Pan, Di Qiu, Shu Chen, Xiaoxue Han, Ruiman Li","doi":"10.4081/ejh.2023.3691","DOIUrl":"https://doi.org/10.4081/ejh.2023.3691","url":null,"abstract":"<p><p>The high prevalence of prediabetes and diabetes globally has led to the widespread occurrence of severe complications, such as diabetic neuropathy, which is a result of chronic hyperglycemia. Studies have demonstrated that maternal diabetes can lead to neural tube defects by suppressing neurogenesis during neuroepithelium development. While aberrant autophagy has been associated with abnormal neuronal differentiation, the mechanism by which high glucose suppresses neural differentiation in stem cells remains unclear. Therefore, we developed a neuronal cell differentiation model of retinoic acid induced P19 cells to investigate the impact of high glucose on neuronal differentiation in vitro. Our findings indicate that high glucose (HG) hinders neuronal differentiation and triggers excessive. Furthermore, HG treatment significantly reduces the expression of markers for neurons (Tuj1) and glia (GFAP), while enhancing autophagic activity mediated by peroxisome proliferator-activated receptor gamma (PPARγ). By manipulating PPARγ activity through pharmacological approaches and genetically knocking it down using shRNA, we discovered that altering PPARγ activity affects the differentiation of neural stem cells exposed to HG. Our study reveals that PPARγ acts as a downstream mediator in high glucose-suppressed neural stem cell differentiation and that refining autophagic activity via PPARγ at an appropriate level could improve neuronal differentiation efficiency. Our data provide novel insights and potential therapeutic targets for the clinical management of gestational diabetes mellitus.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3e/19/ejh-67-2-3691.PMC10230556.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9931775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang
{"title":"Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway.","authors":"Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang","doi":"10.4081/ejh.2023.3653","DOIUrl":"https://doi.org/10.4081/ejh.2023.3653","url":null,"abstract":"<p><p>The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3b/42/ejh-67-2-3653.PMC10230553.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9559623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti
{"title":"<b>RETRACTION</b>: Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus.","authors":"Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti","doi":"10.4081/ejh.2023.3765","DOIUrl":"https://doi.org/10.4081/ejh.2023.3765","url":null,"abstract":"<p><p>On behalf of the coauthors and with much regret, I must retract our publication entitled \"Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus\" published in European Journal of Histochemistry 2010;54(2):e17 for the following reason: Unfortunately, now, after thirteen years, we have realized that some microphotographs published in the paper have been processed to improve the presentation of the images. The three surviving authors of the paper agree that the processing of the presentation images is against the COPE Ethical Editorial Standard, although the presentation images do not alter the integrity of methodological procedures and the results of the research work, obtained from the direct analysis of slides under microscope and rigorous statistical analysis of data; therefore, we, the authors of the above indicated paper, request the retraction of the publication. We apologize for what happened. Maurizio Sabbatini Dip. di Scienze e Innovazione Tecnologica (DISIT) Università del Piemonte Orientale Alessandria, Italy.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a2/17/ejh-67-2-3765.PMC10203977.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9519597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhanshu Ma, Qi Gao, Wenjing Xin, Lei Wang, Yan Chen, Chang Su, Songyan Gao, Ruiling Sun
{"title":"The role of miR-143-3p/FNDC1 axis on the progression of non-small cell lung cancer.","authors":"Zhanshu Ma, Qi Gao, Wenjing Xin, Lei Wang, Yan Chen, Chang Su, Songyan Gao, Ruiling Sun","doi":"10.4081/ejh.2023.3577","DOIUrl":"https://doi.org/10.4081/ejh.2023.3577","url":null,"abstract":"<p><p>The study aimed to explore the functional role of fibronectin type III domain containing 1 (FNDC1) in nonsmall cell lung cancer (NSCLC), as well as the mechanism governing its expression. The expression levels of FNDC1 and related genes in tissue and cell samples were detected by qRT-PCR. Kaplan-Meier analysis was employed to analyze the association between FNDC1 level and the overall survival of NSCLC patients. Functional experiments such as CCK-8 proliferation, colony formation, EDU staining, migration and invasion assays were conducted to investigate the functional role of FNDC1 in regulating the malignancy of NSCLC cells. Bioinformatic tools and dual-luciferase reporter assay were used to identify the miRNA regulator of FNDC1 in NSCLC cells. Our data revealed the upregulation of FNDC1 at mRNA and protein levels in NSCLC tumor tissues cancer cell lines, compared with normal counterparts. NSCLC patients with higher FNDC1 expression suffered from a poorer overall survival. FNDC1 knockdown significantly suppressed the proliferation, migration and invasion of NSCLC cells, and had an inhibitory effect on tube formation. We further demonstrated that miR-143-3p was an upstream regulator of FNDC1 and miR-143-3p expression was repressed in NSCLC samples. Similar to FNDC1 knockdown, miR-143-3p overexpression inhibited the growth, migration and invasion of NSCLC cells. FNDC1 overexpression could partially rescue the effect of miR-143-3p overexpression. FNDC1 silencing also suppressed the tumorigenesis of NSCLC cells in mouse model. In conclusion, FNDC1 promotes the malignant prototypes of NSCLC cells. miR-143-3p is a negative regulator of FNDC1 in NSCLC cells, which may serve as a promising therapeutic target in NSCLC.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4a/43/ejh-67-2-3577.PMC10203978.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10299164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Clinicopathological assessment of PD-1/PD-L1 immune checkpoint expression in desmoid tumors.","authors":"Kazuhiko Hashimoto, Shunji Nishimura, Yu Shinyashiki, Tomohiko Ito, Ryosuke Kakinoki, Masao Akagi","doi":"10.4081/ejh.2023.3688","DOIUrl":"https://doi.org/10.4081/ejh.2023.3688","url":null,"abstract":"<p><p>The details of immune molecules' expression in desmoid tumors (DTs) remain unclear. This study aimed to determine the expression status of the programmed death-1/programmed death ligand 1 (PD1/PD-L1) immune checkpoint mechanism in DTs. The study included patients with DTs (n=9) treated at our institution between April 2006 and December 2012. Immunostaining for CD4, CD8, PD-1, PD-L1, interleukin-2 (IL-2), and interferon-gamma (IFN-γ) was performed on pathological specimens harvested during the biopsy. The positivity rate of each immune component was calculated as the number of positive cells/total cells. The positivity rate was quantified and correlations between the positivity rates of each immune molecule were also investigated. Immune molecules other than PD-1 were stained in tumor cells and intra-tumor infiltrating lymphocytes. The mean ± SD expression rates of β-catenin, CD4, CD8, PD-1, PD-L1, IL-2, and IFN-ɤ were 43.9±18.9, 14.6±6.80, 0.75±4.70, 0±0, 5.1±6.73, 8.75±6.38, and 7.03±12.1, respectively. The correlation between β-catenin and CD4 was positively moderate (r=0.49); β-catenin and PD-L1, positively weak (r=0.25); CD4 and PD-L1, positively medium (r=0.36); CD8 and IL-2, positively medium (r=0.38); CD8 and IFN-ɤ, positively weak (r=0.28); and IL-2 and IFN-ɤ, positively medium (r=0.36). Our findings suggest that PD-L1-centered immune checkpoint mechanisms may be involved in the tumor microenvironment of DTs.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e7/df/ejh-67-2-3688.PMC10184173.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9467135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
David Cajas, Emanuel Guajardo, Sergio Jara-Rosales, Claudio Nuñez, Renato Vargas, Victor Carriel, Antonio Campos, Luis Milla, Pedro Orihuela, Carlos Godoy-Guzman
{"title":"Molecules involved in the sperm interaction in the human uterine tube: a histochemical and immunohistochemical approach.","authors":"David Cajas, Emanuel Guajardo, Sergio Jara-Rosales, Claudio Nuñez, Renato Vargas, Victor Carriel, Antonio Campos, Luis Milla, Pedro Orihuela, Carlos Godoy-Guzman","doi":"10.4081/ejh.2023.3513","DOIUrl":"https://doi.org/10.4081/ejh.2023.3513","url":null,"abstract":"<p><p>In humans, even where millions of spermatozoa are deposited upon ejaculation in the vagina, only a few thousand enter the uterine tube (UT). Sperm transiently adhere to the epithelial cells lining the isthmus reservoir, and this interaction is essential in coordinating the availability of functional spermatozoa for fertilization. The binding of spermatozoa to the UT epithelium (mucosa) occurs due to interactions between cell-adhesion molecules on the cell surfaces of both the sperm and the epithelial cell. However, in humans, there is little information about the molecules involved. The aim of this study was to perform a histological characterization of the UT focused on determining the tissue distribution and deposition of some molecules associated with cell adhesion (F-spondin, galectin-9, osteopontin, integrin αV/β3) and UT's contractile activity (TNFα-R1, TNFα-R2) in the follicular and luteal phases. Our results showed the presence of galectin-9, F-spondin, osteopontin, integrin αV/β3, TNFα-R1, and TNFα-R2 in the epithelial cells in ampullar and isthmic segments during the menstrual cycle. Our results suggest that these molecules could form part of the sperm-UT interactions. Future studies will shed light on the specific role of each of the identified molecules.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/82/4d/ejh-67-2-3513.PMC10141343.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9361292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qian Hu, Ran Tao, Xiaoyun Hu, Haibo Wu, Jianjun Xu
{"title":"Effects of piperlonguminine on lung injury in severe acute pancreatitis <em>via</em> the TLR4/NF-κB pathway.","authors":"Qian Hu, Ran Tao, Xiaoyun Hu, Haibo Wu, Jianjun Xu","doi":"10.4081/ejh.2023.3639","DOIUrl":"10.4081/ejh.2023.3639","url":null,"abstract":"<p><p>Acute pancreatitis is an inflammatory response in the pancreas, involving activation of pancreatic enzymes. Severe acute pancreatitis (SAP) often causes systemic complications that affect distant organs, including the lungs. The aim of this study was to explore the therapeutic potential of piperlonguminine on SAP-induced lung injury in rat models. Acute pancreatitis was induced in rats by repetitive injections with 4% sodium taurocholate. Histological examination and biochemical assays were used to assess the severity of lung injury, including tissue damage, and levels of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4), reactive oxygen species (ROS), and inflammatory cytokines. We found that piperlonguminine significantly ameliorated pulmonary architectural distortion, hemorrhage, interstitial edema, and alveolar thickening in rats with SAP. In addition, NOX2, NOX4, ROS, and inflammatory cytokine levels in pulmonary tissues were notably decreased in piperlonguminine-treated rats. Piperlonguminine also attenuated the expression levels of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB). Together, our findings demonstrate for the first time that piperlonguminine can ameliorate acute pancreatitis-induced lung injury via inhibitory modulation of inflammatory responses by suppression of the TLR4/NF-κB signaling pathway.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b1/91/ejh-67-2-3639.PMC10080291.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9650550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Nrf2 as a novel diagnostic biomarker for papillary thyroid carcinoma.","authors":"Zhiyang Wang, Jing Li, Ziwei Liu, Ling Yue","doi":"10.4081/ejh.2023.3622","DOIUrl":"https://doi.org/10.4081/ejh.2023.3622","url":null,"abstract":"<p><p>Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy. However, it is very difficult to distinguish PTC from benign carcinoma. Thus, specific diagnostic biomarkers are actively pursued. Previous studies observed that Nrf2 was highly expressed in PTC. Based on this research, we hypothesized that Nrf2 may serve as a novel specific diagnostic biomarker. A single-center retrospective study, including 60 patients with PTC and 60 patients with nodular goiter, who underwent thyroidectomy at the Central Theater General Hospital from 2018 to July 2020, was conducted. The clinical data of the patients were collected. Nrf2, BRAF V600E, CK-19, and Gal-3 proteins were compared from paraffin samples of the patients. Through this study, we obtained the following results: i) Nrf2 exhibits high abundance expression in PTC, but not in adjacent to PTC and nodular goiter; increased Nrf2 expression could serve as a valuable biomarker for PTC diagnosis; the sensitivity and specificity for the diagnosis of PTC were 96.70% and 89.40%, respectively. ii) Nrf2 also shows higher expression in PTC with lymph node metastasis, but not adjacent to PTC and nodular goiter, thus the increased Nrf2 expression might serve as a valuable predictor for lymph node metastasis in PTC patients; the sensitivity and specificity for the prediction in lymph node metastasis were 96.00% and 88.57%, respectively; excellent diagnostic agreements were found between Nrf2 and other routine parameters including HO-1, NQO1 and BRAF V600E. iii) The downstream molecular expression of Nrf2 including HO-1 and NQO1 consistently increased. In conclusion, Nrf2 displays a high abundance expression in human PTC, which leads to the higher expression of downstream transcriptional proteins: HO-1 and NQO1. Moreover, Nrf2 can be used as an extra biomarker for differential diagnosis of PTC and a predictive biomarker for lymph node metastasis of PTC.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bb/c5/ejh-67-2-3622.PMC10080292.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9281290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhi Wang, Guihua Jian, Teng Chen, Yiping Chen, Junhui Li, Niansong Wang
{"title":"The Qi-Bang-Yi-Shen formula ameliorates renal dysfunction and fibrosis in rats with diabetic kidney disease <em>via</em> regulating PI3K/AKT, ERK and PPARγ signaling pathways.","authors":"Zhi Wang, Guihua Jian, Teng Chen, Yiping Chen, Junhui Li, Niansong Wang","doi":"10.4081/ejh.2023.3648","DOIUrl":"https://doi.org/10.4081/ejh.2023.3648","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and a growing public health problem worldwide. Losartan potassium (Los), an angiotensin II receptor blocker, has been used to treat DKD clinically. Recently, multi-herbal formula has been shown to exhibit therapeutic activities in DKD in China. Thus, we aimed to explore the protective effects of combination of Los and Qi-Bang-Yi-Shen formula (QBF) on DKD rats. Streptozotocin (STZ) injection was used to establish a rat model of DKD. Next, the bloodurea nitrogen (BUN), creatinine (CRE) and uric acid (UA) levels were detected in serum samples from DKD rats. Hematoxylin and eosin (H&E), periodic Acid Schiff (PAS) and Masson staining were performed to observe glomerular injury and glomerular fibrosis in DKD rats. In this study, we found that QBF or Los treatment could decrease serum BUN, CRE, UA levels and reduce urine albumin-to-creatinine ratio (ACR) in DKD rats. Additionally, QBF or Los treatment obviously inhibited glomerular mesangial expansion and glomerular fibrosis, attenuated glomerular injury in kidney tissues of DKD rats. Moreover, QBF or Los treatment significantly reduced PI3K, AKT and ERK1/2 protein expressions, but increased PPARγ level in kidney tissues of DKD rats. As expected, combined treatment of QBF and Los could exert enhanced reno-protective effects compared with the single treatment. Collectively, combination of QBF and Los could ameliorate renal injury and fibrosis in DKD rats via regulating PI3K/AKT, ERK and PPARγ signaling pathways. These findings highlight the therapeutic potential of QBF to prevent DKD progression.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0b/e2/ejh-67-1-3648.PMC10300429.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10081625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 contribution of immunohistochemistry to the development of hydrogels for skin repair and regeneration.","authors":"Flavia Carton","doi":"10.4081/ejh.2023.3679","DOIUrl":"https://doi.org/10.4081/ejh.2023.3679","url":null,"abstract":"<p><p>Hydrogels based on various polymeric materials have been successfully developed in recent years for a variety of skin applications. Several studies have shown that hydrogels with regenerative, antibacterial, and antiinflammatory properties can provide faster and better healing outcomes, particularly in chronic diseases where the normal physiological healing process is significantly hampered. Various experimental tests are typically performed to assess these materials' ability to promote angiogenesis, re-epithelialization, and the production and maturation of new extracellular matrix. Immunohistochemistry is important in this context because it allows for the visualization of in situ target tissue factors involved in the various stages of wound healing using antibodies labelled with specific markers detectable with different microscopy techniques. This review provides an overview of the various immunohistochemical techniques that have been used in recent years to investigate the efficacy of various types of hydrogels in assisting skin healing processes. The large number of scientific articles published demonstrates immunohistochemistry's significant contribution to the development of engineered biomaterials suitable for treating skin injuries.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a0/b0/ejh-67-1-3679.PMC10300430.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10062244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}