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Obligatory role of Schwann cell‐specific erythropoietin receptors in erythropoietin‐induced functional recovery and neurogenic muscle atrophy after nerve injury
Author(s) -
Talukder M A Hassan,
Lee Jung Il,
Hegarty John P.,
Gurjar Anagha A.,
O'Brien Mary,
Karuman Zara,
Wandling Grant D.,
Govindappa Prem Kumar,
Elfar John C.
Publication year - 2021
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.27121
Subject(s) - erythropoietin receptor , erythropoietin , schwann cell , muscle atrophy , knockout mouse , receptor , sciatic nerve , atrophy , endocrinology , medicine , biology , microbiology and biotechnology
Background Erythropoietin (EPO) promotes myelination and functional recovery in rodent peripheral nerve injury (PNI). While EPO receptors ( EpoR ) are present in Schwann cells, the role of EpoR in PNI recovery is unknown because of the lack of EpoR antagonists or Schwann cell‐specific EpoR knockout animals. Methods Using the Cre‐loxP system, we developed a myelin protein zero (Mpz) promoter‐driven knockout mouse model of Schwann cell EpoR ( MpzCre‐EpoR flox/flox , Mpz‐EpoR‐KO ). Mpz‐EpoR‐KO and control mice were assigned to sciatic nerve crush injury followed by EPO treatment. Results EPO treatment significantly accelerated functional recovery in control mice in contrast to significantly reduced functional recovery in Mpz‐EpoR‐KO mice. Significant muscle atrophy was found in the injured hindlimb of EPO‐treated Mpz‐EpoR‐KO mice but not in EPO‐treated control mice. Conclusions These preliminary findings provide direct evidence for an obligatory role of Schwann‐cell specific EpoR for EPO‐induced functional recovery and muscle atrophy following PNI.