BMP-8b
BMP-8 is a pleiotropic ligand protein act as a reproductive system regulator. BMP-8 is encoded by a pair of genes, BMP8A and BMP8B, belonging to TNF-β family. GMP-8 initiates the canonical BMP signaling cascade by associating with type I receptor BMPR1A and type II receptor BMPR2. Both BMP8A and BMP8B are enriched in the ovary and activate canonical BMP signaling in different cells, including spermatogonia, P19 and 293T cells[1]. BMP-8 is widely found in different animals, while the sequences of BMP-8A and BMP-8B in human are highly different from Mouse with similarities of 85.96% and 74.44%, respectively. As for BMP8B, which protein is secreted by brown/beige adipocytes and enhances energy dissipation, serves as an interconnected regulator of neuro-vascular remodeling in AT and is potential targets in obesity[2]. BMP8B increases brown adipose tissue thermogenesis through both central and peripheral actions[3]. Thus BMP8B contributes to adrenergic-induced remodeling of the neuro-vascular network in adipose tissue, therefore through the adipocytes to 1) secrete neuregulin-4 (NRG4), which promotes sympathetic axon growth and branching in vitro, and 2) induce a pro-angiogenic transcriptional and secretory profile that promotes vascular sprouting[2]. BMP8B also involve in activation of caspase-3 and -9, and apoptosis to inhibit pancreatic cancer cell growth[4].
- [1]. Wu FJ, et al. Human BMP8A suppresses luteinization of rat granulosa cells via the SMAD1/5/8 pathway. Reproduction. 2020 Mar;159(3):315-324. [Content Brief]
- [2]. Pellegrinelli V, et al. Adipocyte-secreted BMP8b mediates adrenergic-induced remodeling of the neuro-vascular network in adipose tissue. Nat Commun. 2018 Nov 26;9(1):4974. [Content Brief]
- [3]. Whittle AJ, et al. BMP8B increases brown adipose tissue thermogenesis through both central and peripheral actions. Cell. 2012 May 11;149(4):871-85. [Content Brief]
- [4]. Cheng Z, et al. BMP8B mediates the survival of pancreatic cancer cells and regulates the progression of pancreatic cancer. Oncol Rep. 2014 Nov;32(5):1861-6. [Content Brief]