MilliporeSigma
  • Home
  • Search Results
  • Pharmacological inhibition of myostatin improves skeletal muscle mass and function in a mouse model of stroke.

Pharmacological inhibition of myostatin improves skeletal muscle mass and function in a mouse model of stroke.

Scientific reports (2017-10-27)
Marine Maud Desgeorges, Xavier Devillard, Jérome Toutain, Josiane Castells, Didier Divoux, David Frédéric Arnould, Christopher Haqq, Myriam Bernaudin, Anne-Cécile Durieux, Omar Touzani, Damien Gilles Freyssenet
ABSTRACT

In stroke patients, loss of skeletal muscle mass leads to prolonged weakness and less efficient rehabilitation. We previously showed that expression of myostatin, a master negative regulator of skeletal muscle mass, was strongly increased in skeletal muscle in a mouse model of stroke. We therefore tested the hypothesis that myostatin inhibition would improve recovery of skeletal muscle mass and function after cerebral ischemia. Cerebral ischemia (45 minutes) was induced by intraluminal right middle cerebral artery occlusion (MCAO). Swiss male mice were randomly assigned to Sham-operated mice (n = 10), MCAO mice receiving the vehicle (n = 15) and MCAO mice receiving an anti-myostatin PINTA745 (n = 12; subcutaneous injection of 7.5 mg.kg-1 PINTA745 immediately after surgery, 3, 7 and 10 days after MCAO). PINTA745 reduced body weight loss and improved body weight recovery after cerebral ischemia, as well as muscle strength and motor function. PINTA745 also increased muscle weight recovery 15 days after cerebral ischemia. Mechanistically, the better recovery of skeletal muscle mass in PINTA745-MCAO mice involved an increased expression of genes encoding myofibrillar proteins. Therefore, an anti-myostatin strategy can improve skeletal muscle recovery after cerebral ischemia and may thus represent an interesting strategy to combat skeletal muscle loss and weakness in stroke patients.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-α-Tubulin antibody produced in mouse, clone B-5-1-2, ascites fluid
Sigma-Aldrich
Anti-ATG5 (N-terminal) antibody produced in rabbit, affinity isolated antibody, PBS solution
Sigma-Aldrich
Anti-ATG13 antibody produced in rabbit, ~1.0 mg/mL, affinity isolated antibody
Sigma-Aldrich
Anti-p62/SQSTM1 antibody produced in rabbit, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution