Author Correction: Asperosaponin VI promotes angiogenesis and accelerates wound healing in rats via up-regulating HIF-1α/VEGF signaling

Background. The incidence of bone fracture and bone-related diseases is increasing every year. Angiogenesis plays a vital role in fracture healing and bone repair. This study assessed the benefits of Taohong Siwu (TSW) decoction on angiogenesis in isolated rat aortic endothelial cells (RAEC) treated with TSW-containing serum. Methods. The components of TSW decoction were analyzed by liquid chromatography-mass spectrometry (LC-MS). TSW-containing serum was prepared by gavage of TSW decoction to Sprague-Dawley (SD) rats. The effects of TSW-containing serum on the viability, migration, wound healing, and angiogenesis of RAEC were detected by the MTT, transwell, wound healing, and Matrigel lumen formation assays, respectively. In addition, the effects of an HIF-1α inhibitor on TSW-containing serum-induced RAEC were also assessed. The effects of TSW-containing serum on the expression of the HIF-1α signaling pathway were evaluated by qRT-PCR and western blot analysis. Results. LC-MS revealed that TSW decoction primarily contained isomaltulose, choline, D-gluconic acid, L-pipecolic acid, hypotaurine, albiflorin, and tryptophan. TSW-containing serum significantly increased the viability, migration, wound healing, and angiogenesis of RAEC in a dose-dependent manner. Furthermore, our results demonstrated that HIF-1α and VEGF expressions were increased in the cells of TSW-containing serum groups, whereas VHL expression was decreased. The effects of TSW-containing serum were reversed by treatment with an HIF-1α inhibitor. Conclusion. These results suggested that TSW decoction enhanced angiogenesis by regulating the VHL/HIF-1α/VEGF signaling pathway.

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Impact of hypoxia induced VEGF and its signaling during caudal fin regeneration in Zebrafish

10.1101/105767 ◽

2017 ◽

Cited By ~ 1

Author(s):

sagayaraj.R Vivek ◽

R. Malathi

Keyword(s):

Wound Healing ◽

Blood Vessel ◽

Cobalt Chloride ◽

Adult Zebrafish ◽

Caudal Fin ◽

Fin Regeneration ◽

Blood Vessel Formation ◽

Vessel Formation ◽

Vegf Signaling ◽

Fin Length

ABSTRACT:Hypoxia is known to play important role during various cellular process, including regeneration. Regeneration is a complex process involving wound healing and tissue repair. We propose that hypoxia might mediate regeneration through angiogenesis involving angiogenic factors such as VEGF, VEGF-R2, NRP1a during the wound healing process. We have chosen Zebrafish model to study the role of hypoxia induced regeneration. Unlike mammals Zebrafish has the ability to regenerate. Hypoxic condition was mimicked using inorganic salt cobalt chloride to study caudal fin regeneration in adult Zebrafish. Intense blood vessel formation, with increased tail fin length experimented at various time points have been observed when adult zebrafish caudal fin partially amputated were exposed to 1% CoCl2. Regeneration is enhanced under hypoxia, with increased VEGF expression. To study the significance of VEGF signaling during wound healing and tissue regeneration, sunitinib well known inhibitor of VEGF receptor is used against CoCl2-induced caudal fin regeneration. Diminished fin length, lowering of blood vessel formation was documented using angioquant software, reduction in mRNA level of hypoxia inducible factors, VEGF and other pro-angiogenic genes such as VEGF, VEGF-R2, NRP1A, FGFR2, ANGPT1 were observed, while reduction in VEGF protein was demonstrated using western blot analysis. Genistein inhibitor of HIF-1α completely arrested regeneration, with suppression of VEGF highlighting the significance of hypoxia induced VEGF signaling during fin regeneration. Our results suggest that hypoxia through HIF-1α might lead to angiogenesis involving VEGF signaling during wound healing and this might throw light on therapeutic efficacy of cobalt chloride during regeneration.

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The Effects of ZD6474, an Inhibitor of VEGF Signaling, on Cutaneous Wound Healing in Mice1

Journal of Surgical Research ◽

10.1016/j.jss.2005.05.006 ◽

2005 ◽

Vol 129 (2) ◽

pp. 251-259 ◽

Cited By ~ 23

Author(s):

Jason Ko ◽

Joel Ross ◽

Hani Awad ◽

Herbert Hurwitz ◽

Bruce Klitzman

Keyword(s):

Wound Healing ◽

Cutaneous Wound Healing ◽

Cutaneous Wound ◽

Vegf Signaling

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Regulating VEGF signaling in platelet concentrates via specific VEGF sequestering

Biomaterials Science ◽

10.1039/c5bm00633c ◽

2016 ◽

Vol 4 (5) ◽

pp. 819-825 ◽

Cited By ~ 4

Author(s):

David G. Belair ◽

Ngoc Nhi Le ◽

William L. Murphy

Keyword(s):

Wound Healing ◽

Growth Factors ◽

Platelet Concentrates ◽

Vegf Signaling

Platelets contain an abundance of growth factors that mimic the composition of the wound healing milieu, and platelet-derived VEGF in particular can negatively influence wound healing if unregulated.

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ultrastructural process of intestinal wound healing

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141494 ◽

1995 ◽

Vol 53 ◽

pp. 1024-1025

Author(s):

Rick L. Vaughn ◽

Shailendra K. Saxena ◽

John G. Sharp

Keyword(s):

Wound Healing ◽

Epithelial Cells ◽

Smooth Muscles ◽

Microscopic Level ◽

Light Microscopic Level ◽

Ileal Mucosa ◽

Wound Model ◽

Serosal Surface ◽

Complex Process ◽

Orderly Fashion

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.

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Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

Clinical Science ◽

10.1042/cs20191102 ◽

2020 ◽

Vol 134 (16) ◽

pp. 2189-2201

Author(s):

Jessica P.E. Davis ◽

Stephen H. Caldwell

Keyword(s):

Wound Healing ◽

Liver Disease ◽

Hepatic Fibrosis ◽

Cell Activation ◽

Stellate Cell ◽

Factor Xa ◽

Clinical Trial Data ◽

Chronic Liver ◽

Healing Response ◽

Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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