Bao-Qiong Lan, Ya-Jun Wang, Sai-Xi Yu, Wei Liu, Yan-Jun Liu
{"title":"Physical effects of 3D microenvironments on confined cell behaviors.","authors":"Bao-Qiong Lan, Ya-Jun Wang, Sai-Xi Yu, Wei Liu, Yan-Jun Liu","doi":"10.1152/ajpcell.00288.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00288.2024","url":null,"abstract":"<p><p>Cell migration is a fundamental and functional cellular process, influenced by complex microenvironment consisting of different cells and extracellular matrix (ECM). Recent research has highlighted that, besides biochemical cues from the microenvironment, physical cues can also greatly alter cellular behavior. However, due to the complexity of the microenvironment, little is known about how the physical interactions between migrating cells and surrounding microenvironment instruct cell movement. Here, we explore various examples of 3D microenvironment reconstruction models in vitro and describe how the physical interplay between migrating cells and the neighboring microenvironment controls cell behavior. Understanding this mechanical cooperation will provide key insights into organ development, regeneration, and tumor metastasis.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiao Feng, Fan Yu, Xin-Liang He, Pei-Pei Cheng, Qian Niu, Li-Qin Zhao, Qian Li, Xiao-Lin Cui, Zi-Heng Jia, Shu-Yi Ye, Li-Mei Liang, Lin-Jie Song, Liang Xiong, Fei Xiang, Xiao-Rong Wang, Wan-Li Ma, Hong Ye
{"title":"CD8<sup>+</sup> tissue-resident memory T cells are essential in bleomycin-induced pulmonary fibrosis.","authors":"Xiao Feng, Fan Yu, Xin-Liang He, Pei-Pei Cheng, Qian Niu, Li-Qin Zhao, Qian Li, Xiao-Lin Cui, Zi-Heng Jia, Shu-Yi Ye, Li-Mei Liang, Lin-Jie Song, Liang Xiong, Fei Xiang, Xiao-Rong Wang, Wan-Li Ma, Hong Ye","doi":"10.1152/ajpcell.00368.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00368.2024","url":null,"abstract":"<p><p>Human tissue-resident memory T (T<sub>RM</sub>) cells play a crucial role in protecting the body from infections and cancers. Recent research observed increased numbers of T<sub>RM</sub> cells in the lung tissues of idiopathic pulmonary fibrosis patient. However, the functional consequences of T<sub>RM</sub> cells in pulmonary fibrosis remain unclear. Here, we found that the numbers of T<sub>RM</sub> cells, especially the CD8<sup>+</sup> subset, were increased in the mouse lung with bleomycin-induced pulmonary fibrosis. Increasing or decreasing CD8<sup>+</sup> T<sub>RM</sub> cells in mouse lungs accordingly altered the severity of fibrosis. In addition, adoptive transfer of CD8<sup>+</sup> T cells containing a large number of CD8<sup>+</sup> T<sub>RM</sub> cells from fibrotic lungs was sufficient to induce pulmonary fibrosis in control mice. Treatment with CCL18 to induced CD8<sup>+</sup> T<sub>RM</sub> cell expansion and exacerbated fibrosis, while blocking CCR8 prevented CD8<sup>+</sup> T<sub>RM</sub> recruitment and inhibited pulmonary fibrosis. In conclusion, CD8<sup>+</sup> T<sub>RM</sub> cells are essential for bleomycin-induced pulmonary fibrosis, and targeting CCL18/CCR8/CD8<sup>+</sup> T<sub>RM</sub> cells may be a potential therapeutic approach.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ting Liu, Jialing Yuan, Caihong Dai, Mystie X Chen, Jerry Fan, Benjamin D. Humphreys, David J. Fulton, Daniel T. Kleven, Xingjun Fan, Zheng Dong, Jian-Kang Chen
{"title":"Pik3c3 Expression Profiling in the Mouse Kidney and Its Role in Proximal Tubule Cell Physiology","authors":"Ting Liu, Jialing Yuan, Caihong Dai, Mystie X Chen, Jerry Fan, Benjamin D. Humphreys, David J. Fulton, Daniel T. Kleven, Xingjun Fan, Zheng Dong, Jian-Kang Chen","doi":"10.1152/ajpcell.00564.2023","DOIUrl":"https://doi.org/10.1152/ajpcell.00564.2023","url":null,"abstract":"American Journal of Physiology-Cell Physiology, Ahead of Print. <br/>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142204166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Selvaraj Anthonymuthu, Subrata Sabui, Kameron I Manzon, Alaullah Sheikh, James M Fleckenstein, Hamid M Said
{"title":"Bacterial lipopolysaccharide inhibits free thiamin uptake along the intestinal tract via interference with membrane expression of thiamin transporters-1 & -2.","authors":"Selvaraj Anthonymuthu, Subrata Sabui, Kameron I Manzon, Alaullah Sheikh, James M Fleckenstein, Hamid M Said","doi":"10.1152/ajpcell.00570.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00570.2024","url":null,"abstract":"<p><p>This study examined the effect of exposure of small and large intestinal epithelial cells to the bacterial lipopolysaccharide (LPS) on uptake of free form of vitamin B1, i.e., thiamin. The intestinal tract encounters two sources of thiamin: diet and the gut microbiota. Absorption of thiamin in both the small and large intestine occurs via a carrier-mediated process that involves thiamin transporters-1 & -2 (THTR-1 & -2). Complementary <i>in vitro</i> (human duodenal epithelial HuTu-80 cells and human colonic epithelial NCM460 cells), <i>in vivo</i> (mice), and <i>ex vivo</i> (human primary differentiated enteroid and colonoid monolayers) models were used. The results showed that exposure to LPS causes a significant inhibition in carrier-mediated [<sup>3</sup>H]-thiamin uptake by small and large intestinal epithelia, with no change in levels of expression of THTR-1& -2 mRNAs and their total cellular proteins. However, a significant decrease in the fractions of the THTR-1& -2 proteins that are expressed at the cell membranes of these epithelial cells was observed. These effects of LPS appeared to involve a protein kinase A (PKA) signaling pathway as activating this pathway caused a reversal in the inhibition of thiamin uptake and level of expression of its transporters at the cell membrane. These findings demonstrate that exposure of gut epithelia to LPS (a situation that occurs under different pathological conditions) leads to inhibition in thiamin uptake due to a decrease in level of expression of its transporters at the cell membrane that is likely mediated via a PKA-signaling pathway.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Corrigendum for Hagen et al., volume 327, 2024, p. C372–C378","authors":"","doi":"10.1152/ajpcell.00326.2024_cor","DOIUrl":"https://doi.org/10.1152/ajpcell.00326.2024_cor","url":null,"abstract":"American Journal of Physiology-Cell Physiology, Volume 327, Issue 3, Page C867-C867, September 2024. <br/>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142204250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jichao Zhang, Zhao Yang, Congcong Zhang, Shijuan Gao, Yan Liu, Yingkai Li, Songyuan He, Jing Yao, Jie Du, Bin You, Yingchun Han
{"title":"PALMD haploinsufficiency aggravates extracellular matrix remodeling in vascular smooth muscle cells and promotes calcification.","authors":"Jichao Zhang, Zhao Yang, Congcong Zhang, Shijuan Gao, Yan Liu, Yingkai Li, Songyuan He, Jing Yao, Jie Du, Bin You, Yingchun Han","doi":"10.1152/ajpcell.00217.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00217.2024","url":null,"abstract":"<p><strong>Background: </strong>Reduced PALMD expression is strongly associated with the development of calcified aortic valve stenosis; however, the role of PALMD in vascular calcification remains unknown.</p><p><strong>Methods: </strong>Calcified arteries were collected from mice to detect PALMD expression. Heterozygous <i>Palmd</i> knockout (<i>Palmd</i><sup>+/-</sup>) mice were established to explore the role of PALMD in subtotal nephrectomy-induced vascular calcification. RNA sequencing was applied to detect molecular changes in aortas from <i>Palmd</i><sup>+/-</sup> mice. Primary <i>Palmd</i><sup>+/-</sup> vascular smooth muscle cells (VSMCs) or PALMD silenced VSMCs by short interfering RNA (siRNA) were used to analyze PALMD function in phenotypic changes and calcification.</p><p><strong>Results: </strong>PALMD haploinsufficiency aggravated subtotal nephrectomy-induced vascular calcification. RNA sequencing analysis showed that loss of PALMD disturbed the synthesis and degradation of the extracellular matrix (ECM) in aortas, including collagens and matrix metalloproteinases (Col6a6, Mmp2, Mmp9, etc.). <i>In vitro</i> experiments revealed that PALMD deficient VSMCs were more susceptible to high phosphate induced calcification. Downregulation of SMAD6 expression and increased levels of p-SMAD2 were detected in <i>Palmd</i><sup>+/-</sup> VSMCs, suggesting that TGF-β signaling may be involved in PALMD haploinsufficiency-induced vascular calcification.</p><p><strong>Conclusion: </strong>Our data revealed that PALMD haploinsufficiency causes ECM dysregulation in VSMCs and aggravates vascular calcification. Our findings suggest reduced PALMD expression is also linked to vascular calcification, and PALMD maybe a potential therapeutic target for this disease.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jacob A Herring, Jacqueline E Crabtree, Jonathon T Hill, Jeffery S Tessem
{"title":"Loss of glucose-stimulated β-cell Nr4a1 expression impairs insulin secretion and glucose homeostasis.","authors":"Jacob A Herring, Jacqueline E Crabtree, Jonathon T Hill, Jeffery S Tessem","doi":"10.1152/ajpcell.00315.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00315.2024","url":null,"abstract":"<p><p>A central aspect of type 2 diabetes is decreased functional β-cell mass. The orphan nuclear receptor Nr4a1 is critical for fuel utilization, but little is known regarding its regulation and function in the β-cell. Nr4a1 expression is decreased in type 2 diabetes rodent β-cells and type 2 diabetes patient islets. We have shown that Nr4a1 deficient mice have reduced β-cell mass and that Nr4a1 knock-down impairs glucose-stimulated insulin secretion (GSIS) in INS-1 832/13 β-cells. Here, we demonstrate that glucose concentration directly regulates β-cell Nr4a1 expression. We show that 11 mM glucose increases Nr4a1 expression in INS-1 832/13 β-cells and primary mouse islets. We show that glucose functions through the cAMP/PKA/CREB pathway to regulate Nr4a1 mRNA and protein expression. Using Nr4a1<sup>-/-</sup> animals, we show that Nr4a1 is necessary for GSIS and systemic glucose handling. Using RNA-seq, we define Nr4a1-regulated pathways in response to glucose in the mouse islet, including Glut2 expression. Our data suggests that Nr4a1 plays a critical role in the β-cells response to the fed state.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}