The low-affinity receptor for neurotrophins p75NTR plays a key role for satellite cell function in muscle repair acting via RhoA.

نویسندگان

  • Daniela Deponti
  • Roberta Buono
  • Giuseppina Catanzaro
  • Clara De Palma
  • Renato Longhi
  • Raffaella Meneveri
  • Nereo Bresolin
  • Maria Teresa Bassi
  • Giulio Cossu
  • Emilio Clementi
  • Silvia Brunelli
چکیده

Regeneration of muscle fibers, lost during pathological muscle degeneration or after injuries, is mediated by the production of new myofibres. This process, sustained by the resident stem cells of the muscle, the satellite cells, is finely regulated by local cues, in particular by cytokines and growth factors. Evidence in the literature suggests that nerve growth factor (NGF) is involved in muscle fiber regeneration; however, its role and mechanism of action were unclear. We have investigated this issue in in vivo mouse models of muscle regeneration and in primary myogenic cells. Our results demonstrate that NGF acts through its low-affinity receptor p75(NTR) in a developmentally regulated signaling pathway necessary to myogenic differentiation and muscle repair in vivo. We also demonstrate that this action of NGF is mediated by the down-regulation of RhoA-GTP signaling in myogenic cells.

برای دانلود رایگان 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

Neurotrophins and Neuropathic Pain: Role in Pathobiology.

Neurotrophins (NTs) belong to a family of trophic factors that regulate the survival, growth and programmed cell death of neurons. In mammals, there are four structurally and functionally related NT proteins, viz. nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 and neurotrophin 4. Most research on NTs to date has focussed on the effects of NGF and BDNF signal...

متن کامل

p75 neurotrophin receptor signaling regulates growth cone filopodial dynamics through modulating RhoA activity.

The mechanisms by which neurotrophins regulate growth cone motility are unclear. We investigated the role of the p75 neurotrophin receptor (p75NTR) in mediating neurotrophin-induced increases in filopodial length. Our data demonstrate that neurotrophin binding to p75NTR is necessary and sufficient to regulate filopodial dynamics. Furthermore, retinal and dorsal root ganglion growth cones from p...

متن کامل

p75 neurotrophin receptor and pro-BDNF promote cell survival and migration in clear cell renal cell carcinoma

p75NTR, a member of TNF receptor family, is the low affinity receptor common to several mature neurotrophins and the high affinity receptor for pro-neurotrophins. Brain-Derived Neurotrophic Factor (BDNF), a member of neurotrophin family has been described to play an important role in development and progression of several cancers, through its binding to a high affinity tyrosine kinase receptor ...

متن کامل

Neurotrophin Binding to the p75 Receptor Modulates Rho Activity and Axonal Outgrowth

While the neurotrophin receptor p75NTR is expressed by many developing neurons, its function in cells escaping elimination by programmed cell death remains unclear. The lack of intrinsic enzymatic activity of p75NTR prompted a search for protein interactors expressed in the developing retina, which resulted in the identification of the GTPase RhoA. In transfected cells, p75NTR activated RhoA, a...

متن کامل

Pro-neurotrophins, sortilin, and nociception

Nerve growth factor (NGF) signaling is important in the development and functional maintenance of nociceptors, but it also plays a central role in initiating and sustaining heat and mechanical hyperalgesia following inflammation. NGF signaling in pain has traditionally been thought of as primarily engaging the classic high-affinity receptor tyrosine kinase receptor TrkA to initiate sensitizatio...

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

عنوان ژورنال:
  • Molecular biology of the cell

دوره 20 16  شماره 

صفحات  -

تاریخ انتشار 2009