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The Ca2+ influx suppression leads to immunosuppression of T-cell proliferation and is linked to conventional protein kinase C (cPKC) activity, particularly cPKCβII. Using progesterone, analogs, and membrane-impermeable conjugates with cPKC modulators, the study tests whether cPKC activation mediates this inhibition.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/the-rapid-activation-of-cpkcii-by-progesterone-results-in-the-negative-regulation-of-ca2-influx-in-human-resting-t-cells/436230/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/the-rapid-activation-of-cpkcii-by-progesterone-results-in-the-negative-regulation-of-ca2-influx-in-human-resting-t-cells/436230.png","ImageObject",300,407,{"name":92,"@type":93},"River Wang","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-31","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":24},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does progesterone affect Ca2+ influx in human resting T cells?","Question",{"text":112,"@type":113},"Progesterone and its analogs suppress Ca2+ influx in a dose-dependent manner in human resting T cells. This suppression reduces PHA-activated sustained calcium signaling measured by fura-2 fluorescence approaches.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What experimental tools were used to probe the mechanism?",{"text":117,"@type":113},"The study used progesterone, its analogs (R5020/Org OD 02-0), and a plasma membrane-impermeable progesterone-bovine serum albumin conjugate to stimulate resting T cells. It also used cPKC inhibitors and PKC downregulation by PMA.",{"name":119,"@type":110,"acceptedAnswer":120},"Which cPKC isoform is implicated in the observed immunosuppression?",{"text":121,"@type":113},"The findings point to cPKCβII. cPKCβII activation mediates Ca2+ influx suppression, supported by attenuation with a βII-specific inhibitor and by parallel loss of Ca2+ influx suppression when cPKCβII expression is reduced after PMA.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},436230,1790845647,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":24,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":34,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144,"preview_page_count":4},1099514067438,"https://ap-avatar.wpscdn.com/avatar/100002539ee87300030?x-image-process=image/resize,m_fixed,w_180,h_180&k=1780474512215547542","J Chin MedAssoc  \nOriginal article  \nThe rapid activation of cPKCβII by progesterone results in the negative regulation of Ca2+ influx inhuman resting T cells  \nVeronica Hui-Chen Lina, Angela Chienb, Eileen Jea Chiena,*  \naDepartment and Institute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, ROC; bDepartment of Biotechnology, School of Health Technology, Ming Chuan University, Taoyuan, Taiwan, ROC  \nAbstract  \nBackground: Progesterone-stimulated rapid suppression of phytohemagglutinin (PHA)-activated sustained membrane Ca2+ influx is revealed by Mn2+ quenching fura-2 fluorescence. Ca2+ influx suppression results in immunosuppression of T-cell proliferation. Downregulation of protein kinase C (PKC) activity by phorbol 12-myristate 13-acetate (PMA) enhances the PHA-activated increase in sustained intracellular Ca2+ concentration ([Ca2+]i) via Ca2+ influx in T cells. Conventional PKC (cPKC) inhibitors also enhance the [Ca2+]i increase in resting T cells caused by progesterone. This study explores whether cPKC activation by progesterone results in suppression of Ca2+ influx in resting T cells.  \nMethods: Progesterone, its analogs (R5020/Org OD 02-0), and plasma membrane-impermeable progesterone-bovine serum albumin conjugate were used to stimulate human resting T cells. Inhibitors and PKC downregulation by PMA were used to investigate whether cPKC affects Ca2+ influx.  \nResults: Progesterone and analogs dose-dependently suppressed Ca2+ influx in T cells. One cPKC inhibitor, Ro318220, attenuated Ca2+ influx suppression, and enhanced the increase in [Ca2+]i caused by progesterone and analogs. U73122 did not affect Ca2+ influx suppression but did decrease the [Ca2+]i increase. Ca2+ influx suppression was not attenuated by the cPKCα/βI isoformselective inhibitor, Go6976, nevertheless, a cPKCβI/βII isoform-selective inhibitor, LY333531 did. Ca2+ influx suppression was attenuated by the cPKCβII-specific inhibitor CGP53353 . After PKC downregulated by PMA, Ca2+ influx suppression by progesterone and analogs was almost abolished in parallel with a massive reduction in cPKCβII expression. This suggests cPKCβII activation by progesterone and analogs mediate Ca2+ influx suppression in resting T cells.  \nConclusion: Nongenomic membrane activation of cPKCβII by progesterone causes immunosuppression via negative regulation of Ca2+ influx into human resting T cells. This prevents resting T-cell activation and proliferation, which protects the fetus from maternal immune attack while decreasing maternal autoimmune disease flare-ups during pregnancy. Thus, cPKCβII modulators might provide a new therapeutic approach to balancing T-cell tolerance and immunity.  \nKeywords: Conventional protein kinase CβII; Human T cells; Membrane calcium influx; Nongenomic; Progesterone  \n1. INTRODUCTION  \nProgesterone drives numerous maternal physiological adaptations on T cells resulting in tolerance rather than immunity, which ensures the acceptance of the semiallogeneic fetus during pregnancy.1 Progesterone is majorly produced by placenta and its concentrations reach high levels there (1–10 μM) and in blood (100–500 nM) during pregnancy.2,3 These higher levels of progesterone maintain an immunotolerogenic  \n* Address correspondence. Prof. Eileen Jea Chien, Department and Institute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, 155, Section 2, Linong Street, Taipei 112, Taiwan, ROC. E-mail address: eileen@nycu. [edu.tw](edu.tw) (E. J. Chien).  \nConflicts of interest: The authors declare that they have no conflicts of interest related to the subject matter or materials discussed in this article.  \nJournal of Chinese Medical Association. (2023) 86: 885-891.  \nReceived June 20, 2023; accepted July 19, 2023.  \ndoi: 10. 1097/JCMA.0000000000000970.  \nCopyright © 2023, the Chinese Medical Association. This is an open access article under the CC BY-NC-ND license ([http://creativecommons.org/lic","cbCaitTRmscVnReD","https://ap.wps.com/l/cbCaitTRmscVnReD","pdf",894762,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusion\n# Introduction","[{\"question\":\"How does progesterone affect Ca2+ influx in human resting T cells?\",\"answer\":\"Progesterone and its analogs suppress Ca2+ influx in a dose-dependent manner in human resting T cells. This suppression reduces PHA-activated sustained calcium signaling measured by fura-2 fluorescence approaches.\"},{\"question\":\"What experimental tools were used to probe the mechanism?\",\"answer\":\"The study used progesterone, its analogs (R5020/Org OD 02-0), and a plasma membrane-impermeable progesterone-bovine serum albumin conjugate to stimulate resting T cells. It also used cPKC inhibitors and PKC downregulation by PMA.\"},{\"question\":\"Which cPKC isoform is implicated in the observed immunosuppression?\",\"answer\":\"The findings point to cPKCβII. cPKCβII activation mediates Ca2+ influx suppression, supported by attenuation with a βII-specific inhibitor and by parallel loss of Ca2+ influx suppression when cPKCβII expression is reduced after PMA.\"}]","The rapid activation of cPKCβII by progesterone results in the negative regulation of Ca2+ influx in human resting T cells | PDF",1790677241,18]