Talin-dependent integrin activation is required for endothelial proliferation and postnatal angiogenesis

Pulous, Fadi E.; Carnevale, Jamie C.; Al‐Yafeai, Zaki; Pearson, Brenna H.; Hamilton, Jamie A.G.; Henry, Curtis J.; Orr, A. Wayne; Petrich, Brian G.

doi:10.1007/s10456-020-09756-4

Cited by 31 publications

(26 citation statements)

References 40 publications

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“…The activation of p38 MAPK/HIF-1α/VEGF-A exerts anti-apoptotic and angiogenic effects against CIRI (Cheng et al, 2017). The application of MAPK/ERK pathway inhibitors disrupts VEGF-induced angiogenesis, thereby indicating that the MAPK/ERK signaling pathway mediates this process (Pulous et al, 2020). Moreover, hyperbaric oxygen-induced VEGF is activated by C-Jun/ AP-1 and through simultaneously activating the JNK and ERK signaling pathways (Lee et al, 2006).…”

Section: Mapk Pathwaysmentioning

confidence: 99%

Inflammation-Mediated Angiogenesis in Ischemic Stroke

Zhu

Zhang

Zhong

et al. 2021

Front. Cell. Neurosci.

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Stroke is the leading cause of disability and mortality in the world, but the pathogenesis of ischemic stroke (IS) is not completely clear and treatments are limited. Mounting evidence indicate that neovascularization is a critical defensive reaction to hypoxia that modulates the process of long-term neurologic recovery after IS. Angiogenesis is a complex process in which the original endothelial cells in blood vessels are differentiated, proliferated, migrated, and finally remolded into new blood vessels. Many immune cells and cytokines, as well as growth factors, are directly or indirectly involved in the regulation of angiogenesis. Inflammatory cells can affect endothelial cell proliferation, migration, and activation by secreting a variety of cytokines via various inflammation-relative signaling pathways and thus participate in the process of angiogenesis. However, the mechanism of inflammation-mediated angiogenesis has not been fully elucidated. Hence, this review aimed to discuss the mechanism of inflammation-mediated angiogenesis in IS and to provide new ideas for clinical treatment of IS.

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Section: Mapk Pathwaysmentioning

confidence: 99%

Inflammation-Mediated Angiogenesis in Ischemic Stroke

Zhu

Zhang

Zhong

et al. 2021

Front. Cell. Neurosci.

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“…5) [34]. Talin-1 is essential for endothelial proliferation and postnatal angiogenesis [35]. Furthermore, vinculin is a key regulator of cell adhesion by direct interactions with talin and actin (Fig.…”

Section: Discussionmentioning

confidence: 99%

Expression of Thrombin-Cleaved Osteopontin and Integrin α9 and β1 Signaling Pathway Molecules in Chronic Subdural Hematomas

Osuka

Ohmichi

et al. 2021

Preprint

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Chronic subdural hematoma (CSDH) is considered to be an inflammatory and angiogenic disease. Osteopontin is an extracellular matrix protein. Osteopontin is cleaved by thrombin, resulting in N-half osteopontin, which is more prominent in integrin signal transduction. We examined the expression of N-half osteopontin in the CSDH fluid and the expression of integrin α9 and β1 and the downstream components of the angiogenic signaling pathways in the outer membrane of CSDHs. Twenty samples of CSDH fluid and 8 samples of CSDH outer membrane were included. The concentrations of N-half osteopontin in the CSDH fluid were measured using ELISA kits. The expression of integrin α9 and β1, vinculin, talin-1, focal adhesion kinase (FAK), paxillin, α-actin, Src and β-actin was examined by western blot analysis. The expression of integrin α9 and β1, FAK and paxillin was also examined by immunohistochemistry. We investigated whether CSDH fluid could activate FAK in cultured endothelial cells in vitro. The concentration of N-half osteopontin in CSDH fluid was significantly higher than that in the serum. Western blot analysis revealed above-mentioned molecules. In addition, integrin α9 and β1, FAK and paxillin were localized in the endothelial cells of vessels within the CSDH outer membrane. FAK was significantly phosphorylated immediately after treatment with CSDH fluid. Our data suggest that N-half osteopontin in CSDH fluid promotes neovascularization in endothelial cells through integrins α9 and β1. The N-half osteopontin and integrin signaling pathway might be a useful therapeutic target for treating the growth of refractory CSDH.

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“…Talin-1, which is located at the adhesion complex between cells and their extracellular matrix (ECM), has been reported to interact with multiple adhesion molecules and to activate integrin and focal adhesion signaling [7]. Recent studies have indicated that the dysregulation of Talin-1 can lead to cell spreading, migration, and survival, and this has led to an extensive investigation into its role in cancer and other disorders [8][9][10][11][12]. Endometriosis is also a disease with active cell migration and invasion.…”

Section: Introductionmentioning

confidence: 99%

Expression of Talin-1 in endometriosis and its possible role in pathogenesis

Tang

et al. 2021

Reprod Biol Endocrinol

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Background Endometriosis is a disease that involves active cell invasion and migration. Talin-1 can promote cell invasion, migration and adhension in various cancer cells, but its role in endometriosis has not been investigated. This study was to investigate the expression level of Talin-1 in endometriosis and the role of Talin-1 in the proliferation, adhesion, migration, and invasion of human endometrial stromal cells (ESCs). Methods Ectopic and eutopic endometrial tissues were collected from women with endometriosis, and the control endometrial tissues were obtained from patients without endometriosis. The expression level of Talin-1 was detected in each sample using quantitative real-time polymerase chain reaction and immunohistochemistry. The expression of Talin-1 was inhibited using RNA interference in ESCs, and its proliferation, apoptosis, adhesion, migration, and invasion capacity were analyzed. Western blotting was performed to detect the expression of related molecules after the downregulation of Talin-1. Results The results showed that the mRNA and protein expression of Talin-1 were significantly increased in the ectopic endometrium and eutopic endometrial tissues compared with the controls. The knockdown of Talin-1 did not affect the proliferation and apoptosis of ESCs. The results indicated that the downexpression of Talin-1 inhibited the adhesion, invasion, and migration of ESCs. In addition, the expressions of N-cadherin, MMP-2, and integrin β3 were significantly lower after the deregulation of Talin-1, whereas the levels of E-cadherin were significantly increased. Conclusions The expression of Talin-1 was increased in the ectopic and eutopic endometrial tissues compared with the control endometrium. The downregulation of Talin-1 inhibited the adhesion, invasion, and migration of ESCs.

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Talin-dependent integrin activation is required for endothelial proliferation and postnatal angiogenesis

Cited by 31 publications

References 40 publications

Inflammation-Mediated Angiogenesis in Ischemic Stroke

Inflammation-Mediated Angiogenesis in Ischemic Stroke

Expression of Thrombin-Cleaved Osteopontin and Integrin α9 and β1 Signaling Pathway Molecules in Chronic Subdural Hematomas

Expression of Talin-1 in endometriosis and its possible role in pathogenesis

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