Regulation of retinal angiogenesis by endothelial nitric oxide synthase signaling pathway

نویسندگان

  • Jung Min Ha
  • Seo Yeon Jin
  • Hye Sun Lee
  • Hwa Kyoung Shin
  • Dong Hyung Lee
  • Sang Heon Song
  • Chi Dae Kim
  • Sun Sik Bae
چکیده

Angiogenesis plays an essential role in embryo development, tissue repair, inflammatory diseases, and tumor growth. In the present study, we showed that endothelial nitric oxide synthase (eNOS) regulates retinal angiogenesis. Mice that lack eNOS showed growth retardation, and retinal vessel development was significantly delayed. In addition, the number of tip cells and filopodia length were significantly reduced in mice lacking eNOS. Retinal endothelial cell proliferation was significantly blocked in mice lacking eNOS, and EMG-2-induced endothelial cell sprouting was significantly reduced in aortic vessels isolated from eNOS-deficient mice. Finally, pericyte recruitment to endothelial cells and vascular smooth muscle cell coverage to blood vessels were attenuated in mice lacking eNOS. Taken together, we suggest that the endothelial cell function and blood vessel maturation are regulated by eNOS during retinal angiogenesis.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Inducible nitric oxide synthase mediates hypoxia-induced hypoxia-inducible factor-1 alpha activation and vascular endothelial growth factor expression in oxygen-induced retinopathy.

OBJECTIVE Previous studies provided evidence that many factors contribute to retinal angiogenesis, including inducible nitric oxide synthase (iNOS), hypoxia-inducible factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF). But the role of nitric oxide generated by iNOS in the regulation of expression of hypoxia-inducible genes in retinopathy of prematurity remains unclear. S...

متن کامل

Synergistic Effects of Graphene Oxide and Vascular Endothelial Growth Factor Immobilized in Polycaprolactone Nanofiber as a Candidate for Diabetic Wound Healing

   Background & Objective: The combination of two or more therapeutic agents and their synergetic impacts can be therapeutically effective against multifactorial diseases, such as diabetic foot ulcers. This study demonstrates the application of a nanofiber-based drug delivery system with a controlled release of the growth factor. Various studies have shown that vascular endothelial growth facto...

متن کامل

Endothelial Akt1 mediates angiogenesis by phosphorylating multiple angiogenic substrates.

The PI3K/Akt pathway is necessary for several key endothelial cell (EC) functions, including cell growth, migration, survival, and vascular tone. However, existing literature supports the idea that Akt can be either pro- or antiangiogenic, possibly due to compensation by multiple isoforms in the EC when a single isoform is deleted. Thus, biochemical, genetic, and proteomic studies were conducte...

متن کامل

EXPRESSION OF INDUCIBLE NITRIC OXIDE SYNTHASE GENE (iNOS) STIMULATED BY HYDROGEN PEROXIDE IN HUMAN ENDOTHELIAL CELLS

Inducible nitric oxide synthase (iNOS) gene expresses a calcium calmudolin-independent enzyme which can catalyse NO production from L-arginine. The induction of iNOS activity has been demonstrated in a wide variety of cell types under stimulation with cytokines and lipopoly saccharide (LPS). Previous studies indicated that all nitric oxide synthases (NOS) activated in human umbilical vein endot...

متن کامل

Nitric-oxide synthase trafficking inducer is a pleiotropic regulator of endothelial cell function and signaling.

Endothelial nitric-oxide synthase (eNOS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functions, including angiogenesis and vascular permeability. For example, vascular endothelial growth factor (VEGF)-mediated angiogenesis is inhibited upon reduction of NO bioactivity both in vitro and in vivo Moreover, genetic disruption or pharmacological inhibition of eNOS att...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 20  شماره 

صفحات  -

تاریخ انتشار 2016