RNA interference mediated JAM-A gene silencing promotes human epidermal stem cell proliferation

Zhou, Tong; Wu, Minjuan; Guo, Xiaohong; Liu, Houqi

doi:10.1007/s13577-013-0087-2

Cited by 6 publications

(4 citation statements)

References 26 publications

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“…19 Silencing of F11R promoted the migration and proliferation of human keratinocytes and epidermal cells. 20,21 Thus, F11R is not necessary for the migration of lymphocytes and immune cells. F11R is important to maintain the epithelial barrier membrane of the adjacent epithelial cells.…”

Section: Ta B L Ementioning

confidence: 99%

Association of F11R polymorphisms and gene expression with primary Sjögren’s syndrome patients

Fang

Lin

et al. 2021

Int J of Rheum Dis

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F11R gene encodes junctional adhesion molecule-A protein (JAM-A).F11R/JAM-A is a transmembrane glycoprotein which is expressed in various types of cells including epithelial cells, endothelial cells, lymphocytes, monocytes, polymorphonuclear (PMN) cells, dendritic cells and platelets. [1][2][3] The biological function of F11R protein is multifunctional, for instance, F11R is involved in recruiting intracellular signaling, regulating cellular permeability, stimulation of cell translocation during inflammatory processes. 4 F11R is one of the components for cell-cell tight junctions, which maintains the epithelial barrier membrane of the adjacent epithelial cells. F11R serves as an important protein in

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Section: Ta B L Ementioning

confidence: 99%

Association of F11R polymorphisms and gene expression with primary Sjögren’s syndrome patients

Fang

Lin

et al. 2021

Int J of Rheum Dis

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“…Because the cell models were different, the abundance of biochemical molecules within the cells that regulate cell proliferation and migration were different. Our previous studies revealed that silencing JAM‐A promoted human epidermal stem cell proliferation (Zhou et al, 2015), but one of our other studies found that, JAM‐A overexpression strengthened the secretory activity and proliferation of MSCs (Wu et al, 2015). However, the underlying mechanism causing the difference requires further exploration.…”

Section: Discussionmentioning

confidence: 89%

Lentivirus‐mediated subcutaneous JAM‐A modification promotes skin wound healing in a mouse model by strengthening the secretory function and proliferation of fibroblasts

Gong

Wu²,

Fan

et al. 2022

Cell Biology International

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A better understanding of the molecular regulation of wound healing may provide novel therapeutic targets. A previous study revealed that junctional adhesion molecule A (JAM-A)-modified mesenchymal stem cells promoted wound healing.However, whether direct JAM-A modification in the skin wound edge area accelerates the wound repair process is not clear. We determined whether JAM-A modification at the skin wound edge accelerated the wound healing process. We established JAM-A modification mouse wound models and mouse primary fibroblast cell models. Wound pictures were taken to compare the wound size. H&E staining was performed to monitor the morphology of the wound and quality of the newborn skin. CCK-8 assays and immunofluorescence (IF) for Ki67 were used to measure the cell proliferation of mouse primary fibroblasts. Quantitative real-time PCR, immunohistochemistry, IF, and Western blot analysis were used to detect bFGF and EGF expression in vivo and in vitro. The JAM-A-overexpressing group exhibited a smaller residual wound size than the control group at Day 7. Thicker epidermal layers and more hair follicle-like structures were found in the JAM-A-overexpressing group at Day 21. Cell proliferation capacity was higher in JAM-A-modified mouse fibroblasts. Elevated levels of bFGF and EGF were found in the JAM-A-modified group in vivo and in vitro. JAM-A modification significantly promoted fibroblast proliferation and wound healing. Increased levels of bFGF and EGF growth factors may be part of the mechanism.

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“…F11R is a ligand for the integrin LFA1 involved in leukocyte transmigration [66] and is a platelet receptor [67]. In skin, it promotes wound healing by enhancing both homing and secretory activities of MSC [68], regulating also human epidermal stem cell proliferation [69]. Interestingly, it has been also demonstrated that F11R-A2 interactions regulate hematopoietic stem cell fate through Notch signaling [70].…”

Section: Discussionmentioning

confidence: 99%

Intracoronary Delivery of Porcine Cardiac Progenitor Cells Overexpressing IGF-1 and HGF in a Pig Model of Sub-Acute Myocardial Infarction

Crisóstomo

Moscoso

Báez-Díaz

et al. 2021

Cells

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Human cardiac progenitor cells (hCPC) are considered a good candidate in cell therapy for ischemic heart disease, demonstrating capacity to improve functional recovery after myocardial infarction (MI), both in small and large preclinical animal models. However, improvements are required in terms of cell engraftment and efficacy. Based on previously published reports, insulin-growth factor 1 (IGF-1) and hepatocyte growth factor (HGF) have demonstrated substantial cardioprotective, repair and regeneration activities, so they are good candidates to be evaluated in large animal model of MI. We have validated porcine cardiac progenitor cells (pCPC) and lentiviral vectors to overexpress IGF-1 (co-expressing eGFP) and HGF (co-expressing mCherry). pCPC were transduced and IGF1-eGFPpos and HGF-mCherrypos populations were purified by cell sorting and further expanded. Overexpression of IGF-1 has a limited impact on pCPC expression profile, whereas results indicated that pCPC-HGF-mCherry cultures could be counter selecting high expresser cells. In addition, pCPC-IGF1-eGFP showed a higher cardiogenic response, evaluated in co-cultures with decellularized extracellular matrix, compared with native pCPC or pCPC-HGF-mCherry. In vivo intracoronary co-administration of pCPC-IGF1-eGFP and pCPC-HFG-mCherry (1:1; 40 × 106/animal), one week after the induction of an MI model in swine, revealed no significant improvement in cardiac function.

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RNA interference mediated JAM-A gene silencing promotes human epidermal stem cell proliferation

Cited by 6 publications

References 26 publications

Association of F11R polymorphisms and gene expression with primary Sjögren’s syndrome patients

Association of F11R polymorphisms and gene expression with primary Sjögren’s syndrome patients

Lentivirus‐mediated subcutaneous JAM‐A modification promotes skin wound healing in a mouse model by strengthening the secretory function and proliferation of fibroblasts

Intracoronary Delivery of Porcine Cardiac Progenitor Cells Overexpressing IGF-1 and HGF in a Pig Model of Sub-Acute Myocardial Infarction

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