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. 1999 Jan 15;274(3):1525-32.
doi: 10.1074/jbc.274.3.1525.

Induction of high mobility group-I(Y) protein by endotoxin and interleukin-1beta in vascular smooth muscle cells. Role in activation of inducible nitric oxide synthase

A Pellacani  1 , M T Chin, P Wiesel, M Ibanez, A Patel, S F Yet, C M Hsieh, J D Paulauskis, R Reeves, M E Lee, M A Perrella
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Induction of high mobility group-I(Y) protein by endotoxin and interleukin-1beta in vascular smooth muscle cells. Role in activation of inducible nitric oxide synthase

A Pellacani et al. J Biol Chem. .
Free article

Abstract

Nonhistone chromosomal proteins of the high mobility group (HMG) affect the transcriptional regulation of certain mammalian genes. For example, HMG-I(Y) controls cytokine-mediated promoters that require transcription factors, such as nuclear factor-kappaB, for maximal expression. Even though a great deal is known about how HMG-I(Y) facilitates expression of other genes, less is known about the regulation of HMG-I(Y) itself, especially in cells in primary culture. Therefore we investigated the effect of endotoxin and the cytokine interleukin-1beta on HMG-I(Y) expression in vascular smooth muscle cells. Induction of HMG-I(Y) peaked after 48 h of interleukin-1beta stimulation (6.2-fold) in cells in primary culture, and this increase in mRNA corresponded to an increase in HMG-I(Y) protein. Moreover, immunohistochemical staining revealed a dramatic increase in HMG-I(Y) protein expression in vascular smooth muscle cells after endotoxin stimulation in vivo. This increase in HMG-I(Y) expression (both in vitro and in vivo) mirrored an up-regulation of inducible nitric oxide synthase, a cytokine-responsive gene. The functional significance of this coinduction is underscored by our finding that HMG-I(Y) potentiated the response of inducible nitric oxide synthase to nuclear factor-kappaB transactivation. Taken together, these studies suggest that induction of HMG-I(Y), and subsequent transactivation of iNOS, may contribute to a reduction in vascular tone during endotoxemia and other systemic inflammatory processes.

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