First Author | Abudupataer M | Year | 2019 |
Journal | J Cell Mol Med | Volume | 23 |
Issue | 12 | Pages | 8392-8409 |
PubMed ID | 31600036 | Mgi Jnum | J:324745 |
Mgi Id | MGI:7281418 | Doi | 10.1111/jcmm.14720 |
Citation | Abudupataer M, et al. (2019) Histamine deficiency delays ischaemic skeletal muscle regeneration via inducing aberrant inflammatory responses and repressing myoblast proliferation. J Cell Mol Med 23(12):8392-8409 |
abstractText | Histidine decarboxylase (HDC) catalyses the formation of histamine from L-histidine. Histamine is a biogenic amine involved in many physiological and pathological processes, but its role in the regeneration of skeletal muscles has not been thoroughly clarified. Here, using a murine model of hindlimb ischaemia, we show that histamine deficiency in Hdc knockout (Hdc(-/-) ) mice significantly reduces blood perfusion and impairs muscle regeneration. Using Hdc-EGFP transgenic mice, we demonstrate that HDC is expressed predominately in CD11b(+) Gr-1(+) myeloid cells but not in skeletal muscles and endothelial cells. Large amounts of HDC-expressing CD11b(+) myeloid cells are rapidly recruited to injured and inflamed muscles. Hdc(-/-) enhances inflammatory responses and inhibits macrophage differentiation. Mechanically, we demonstrate that histamine deficiency decreases IGF-1 (insulin-like growth factor 1) levels and diminishes myoblast proliferation via H3R/PI3K/AKT-dependent signalling. These results indicate a novel role for HDC-expressing CD11b(+) myeloid cells and histamine in myoblast proliferation and skeletal muscle regeneration. |