Nesfatin-1 inhibits proliferation and enhances apoptosis of human adrenocortical H295R cells

Manjunath Ramanjaneya, Bee K. Tan, Marcin Rucinski, Mohamed Kawan, Jiamiao Hu, Jaspreet Kaur, Vanlata H. Patel, Ludwik K. Malendowicz, Hanna Komarowska, Hendrik Lehnert, Harpal S. Randeva*

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

NUCB2/nesfatin and its proteolytically cleaved product nesfatin-1 are recently discovered anorexigenic hypothalamic neuroproteins involved in energy homeostasis. It is expressed both centrally and in peripheral tissues, and appears to have potent metabolic actions. NUCB2/nesfatin neurons are activated in response to stress. Central nesfatin-1 administration elevates circulating ACTH and corticosterone levels. Bilateral adrenalectomy increased NUCB2/nesfatin mRNA levels in rat paraventricular nuclei. To date, studies have not assessed the effects of nesfatin-1 stimulation on human adrenocortical cells. Therefore, we investigated the expression and effects of nesfatin-1 in a human adrenocortical cell model (H295R). Our findings demonstrate that NUCB2 and nesfatin-1 are expressed in human adrenal gland and human adrenocortical cells (H295R). Stimulation with nesfatin-1 inhibits the growth of H295R cells and promotes apoptosis, potentially via the involvement of Bax, BCL-XL and BCL-2 genes as well as ERK1/2, p38 and JNK1/2 signalling cascades. This has implications for understanding the role of NUCB2/nesfatin in adrenal zonal development. NUCB2/nesfatin may also be a therapeutic target for adrenal cancer. However, further studies using in vivo models are needed to clarify these concepts.

Original languageEnglish
Pages (from-to)1-11
Number of pages11
JournalJournal of Endocrinology
Volume226
Issue number1
Early online date13 Apr 2015
DOIs
Publication statusPublished - Jul 2015

Keywords

  • adrenal cortex
  • apoptosis
  • nesfatin-1
  • NUCB2

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