Methods of increasing myotube formation or survival or muscle cell mitogenesis differentiation or survival using neuregulin GGF III
View Patent ↗The invention relates to methods of treating diseases and disorders of the muscle tissues in a vertebrate by the administration of compounds which bind the p185 erbB2 receptor. These compounds are found to cause increased differentiation and survival of cardiac, skeletal and smooth muscle.
1. The method of increasing the myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival in a mammal in need thereof, said method comprising administering GGF-III polypeptide to said mammal in an amount effective for increasing said myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival.
2. The method of increasing the myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival in a mammal in need thereof, said method comprising administering GGF-III polypeptide to said mammal in an amount effective for decreasing muscle atrophy.
3. The method of claim 1 , wherein said increasing is increasing myotube formation and/or myotube survival.
4. The method of claim 1 , wherein said increasing is increasing the survival of said muscle cell.
5. The method of claim 1 , wherein said increasing results in increased muscle growth in said mammal.
6. The method of claim 1 , wherein said increasing results in increased muscle regeneration in said mammal.
7. The method of increasing the myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival in a mammal in need thereof, said method comprising administering GGF-III polypeptide to said mammal in an amount effective for increasing muscle cell mitogenesis.
8. The method of claim 1 , wherein said increasing further results in increased acetylcholine receptor synthesis.
9. The method of increasing the myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival in a mammal in need thereof, said method comprising administering an effective amount of a GGF-III polypeptide to a mammal lacking a neurotrophic factor.
10. The method of claim 1 , wherein said muscle cell is a myoblast.
11. The method of increasing the myotube formation, myotube survival, muscle cell mitogenesis, or muscle cell survival in a mammal in need thereof, said muscle cell being a satellite cell, said method comprising administering an effective amount of a GGF-III polypeptide to said mammal.
12. The method of claim 1 , wherein said muscle cell is in skeletal muscle.
13. The method of claim 1 , wherein said muscle cell is in cardiac muscle.
14. The method of claim 1 , said muscle cell is in smooth muscle.
15. The method of claim 1 , wherein said mammal has a pathophysiological condition which affects skeletal muscle.
16. The method of claim 15 , wherein said condition is a myopathy.
17. The method of claim 15 , wherein said condition is a dystrophy.
18. The method of claim 17 , wherein said dystrophy is Duchenne's muscular dystrophy.
19. The method of claim 17 , wherein said dystrophy is Becker's dystrophy.
20. The method of claim 15 , wherein said condition is a result of a neural condition.
21. The method of claim 15 , wherein said skeletal muscle is in a mammal which has a traumatic injury.
22. The method of claim 20 , wherein said neural condition is a nerve injury.
23. The method of claim 20 , wherein said neural condition is a neuropathy.
24. The method of claim 1 , wherein said mammal has a pathophysiological condition which affects cardiac muscle.
25. The method of claim 24 , wherein said condition is cardiomyopathy.
26. The method of claim 24 , wherein said condition is ischemic damage.
27. The method of claim 25 , wherein said cardiomyopathy is a degenerative congenital disease.
28. The method of claim 24 , wherein said condition is cardiac trauma.
29. The method of claim 1 , wherein said mammal has a pathophysiological condition which affects smooth muscle.
30. The method of claim 29 , wherein said condition is atherosclerosis.
31. The method of claim 29 , wherein said condition is a vascular lesion.
32. The method of claim 29 , wherein said condition is a degenerative congenital vascular disease.
33. The method of claim 1 , wherein said condition results from insufficient functional acetylcholine receptors in said musculature.
34. The method of claim 33 , wherein said mammal is a patient with myasthenia gravis.
35. The method of claim 1 , wherein said mammal is human.