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BNP is a Novel Regulator of Embryonic Stem Cell Proliferation

Abdelalim,Em,Tooyama

Published 2011 in Unknown venue

ABSTRACT

Embryonic stem (ES) cells are derived from pre-implantation blastocysts. The blastocyst consists of an outer layer of trophoblast cells and an inner cell population called the inner cell mass (ICM). The ICM gives rise to all tissues of the body and some extraembryonic tissues, and it is from these cells that ES cells are derived (Suda et al., 1987). ES cells have two defining properties: self-renewal and pluripotency, and these make them a promising source for cell transplantation therapies (Suda et al., 1987). The precise mechanism that regulates stem cell self-renewal and pluripotency remains largely unknown. Thus investigation into the molecular and cellular mechanisms of stem cell self-renewal and pluripotency provide the necessary tools to harness the regenerative potential of ES cells for therapeutic purposes. The two most striking features related to murine ES cell proliferation rate; (1) their unusual cell cycle structure and (2) their rapid rate of cell division (Savatier et al., 1994; Burdon et al., 2002). Murine ES cells divide with an unusually short generation time of approximately 8-10 hours (Savatier et al., 1994; Burdon et al., 2002), and have unusual cell cycle structure, consist of high proportion of cells in the S phase and, a short G1 phase. Since most cell types spend the majority of their time in G1, the short G1 phase of murine ES cells can account for their rapid rate of cell division since the length of S phase is similar within cell types. The natriuretic peptides (NPs) are a family of three peptides: atrial NP (ANP), brain NP (BNP), and C-type NP (CNP) (Sudoh et al., 1988; Brenner et al., 1990; Sudoh et al., 1990). BNP is produced predominately in the heart (Minamino et al., 1988; Abdelalim et al., 2006a; Abdelalim et al., 2006b). The biological actions of NPs are mediated by binding to cellsurface receptors. These include NP receptor type A (NPR-A or GC-A), which is sensitive to ANP and BNP (Garbers, 1992), NP receptor type B (NPR-B), which is highly specific for CNP (Koller et al., 1991), and NP receptor type C (NPR-C), which comprises up to 95% of the total NPR population (Maack, 1992) and is known to bind all NPs with similar affinity (Levin et al. 1998). Hormone binding to NPR-A and NPR-B activates guanylyl cyclase (GC) and produces cyclic guanosine monophosphate (cGMP), the secondary messenger for a number of biological responses associated with NPs (Garber, 1992; Potter et al., 2006). NPs are released into the circulation from cardiac cells to act as hormones to control fluid volume homeostasis and blood pressure by causing natriuresis, diuresis, vasorelaxation and inhibition of the renin–angiotensin–aldosterone system (Minamino et al., 1988; Abdelalim et

PUBLICATION RECORD

  • Publication year

    2011

  • Venue

    Unknown venue

  • Publication date

    2011-04-26

  • Fields of study

    Biology, Medicine

  • Identifiers
    DOI 10.5772/14832
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar

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