Myeloid cell-derived catecholamines influence bone turnover and regeneration in mice.

ABSTRACT: Catecholamine signaling is known to influence bone tissue as reuptake of norepinephrine released from sympathetic nerves into bone cells declines with age leading to osteoporosis. Further, β-adrenoceptor-blockers like propranolol provoke osteoprotective effects in osteoporotic patients. However, besides systemic adrenal and sympathetic catecholamine production, it is also known that myeloid cells can synthesize catecholamines, especially under inflammatory conditions. To investigate the effects of catecholamines produced by CD11b⁺ myeloid cells on bone turnover and regeneration, a mouse line with specific knockout of tyrosine hydroxylase, the rate-limiting enzyme of catecholamine synthesis, in CD11b⁺ myeloid cells (TH^flox/flox/CD11b-Cre⁺, referre

SUBMITTER: Kuhn MR 

PROVIDER: S-EPMC9520980 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature