ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Knockdown of the KINDLIN-2 Gene and Reduced Expression of Kindlin-2 Affects Vascular Permeability in Angiogenesis in a Mouse Model of Wound Healing.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Kindlin-2 controls angiogenesis through modulating Notch1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- The optimization of PLGA knitted mesh reinforced-collagen/chitosan scaffold for the healing of full-thickness skin defects.Journal of biomedical materials research. Part B, Applied biomaterials · 2023Article
- Article
- Fermitin family homolog 2 (Kindlin-2) affects vascularization during the wound healing process by regulating the Wnt/β-catenin signaling pathway in vascular endothelial cells.Bioengineered · 2021Article
- The Genomes of Two Billfishes Provide Insights into the Evolution of Endothermy in Teleosts.Molecular biology and evolution · 2021Article
- Kindlin-2 regulates the differentiation of 3T3-L1 preadipocytes: implications for wound healing.Annals of translational medicine · 2021Article
- Involvement of kindlin-2 in irisin's protection against ischaemia reperfusion-induced liver injury in high-fat diet-fed mice.Journal of cellular and molecular medicine · 2020Article
- Elevated kindlin-2 promotes tumour progression and angiogenesis through the mTOR/VEGFA pathway in melanoma.Aging · 2019Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Angiogenesis is an important component of wound healing and tissue repair. Kindlin-2 is an integrin-associated protein, encoded by the KINDLIN-2 gene, which has been shown to affect cell adhesion and migration of cells, including endothelial cells. The aim of this study was to use a mouse model of wound healing to evaluate the effects of expression of KINDLIN-2 on angiogenesis in wound healing in vivo. MATERIAL AND METHODS Thirty-six male C57BL/6 mice were studied in an established model that used a wound created on the back. Mice were divided randomly into three groups: the normal group (n=12) received injections of normal (0.9%) saline; the KINDLIN-2(-) group (n=12) received injections of adeno-associated virus with small interfering (si)RNA targeting the KINDLIN-2 gene (AAV-KINDLIN-2-siRNA); and the control (group (n=12) received injections of adeno-associated virus containing a scrambled RNA sequence (AAV-control-RNA). Wound healing was analyzed by biochemical examination of the exudates and histology. Evans blue dye was injected into the caudal vein of each mouse, two weeks after wound healing to assess neovascular permeability. RESULTS Wound healing was significantly delayed in the KINDLIN-2 gene knockdown mice (AAV-KINDLIN-2-siRNA) compared with that of the normal group and the control group, and neovascular permeability was increased. In the AAV-KINDLIN-2-siRNA group, blood vessels were shorter and thinner compared with the normal group and the control group. CONCLUSIONS In a mouse model of wound healing, KINDLIN-2 gene knockdown inhibited wound healing, and increased neovascular permeability in vivo.
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