Extended Abstracts of Invited Lectures

Lang, Frank; Hörl, W.H.; Rosenkranz, Amanda; Kramer, Herbert J.; Häuser, Ivan; Pavenstädt, H.

doi:10.1159/000025977

Cited by 2 publications

(4 citation statements)

References 1 publication

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“…NO has been associated with several intracellular signaling cascades [10, 11, 12, 13]. One such family of signaling proteins is the MAPKs.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…NO has been demonstrated to have an effect on many of these pathways [10, 11, 12, 13]. It utilizes both cyclic guanosine monophosphate (cGMP)-dependent and -independent mechanisms [10, 12, 14]. NO has been shown to upregulate the cyclin-dependent kinase (cdk) inhibitor p21 waf1/cip1 [15, 16, 17], a protein whose antimitotic effects are well described in a variety of cells.…”

Section: Introductionmentioning

confidence: 99%

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Exogenous Nitric Oxide Upregulates p21<sup>waf1/cip1</sup> in Pulmonary Microvascular Smooth Muscle Cells

Stotz

Johns³

2004

J Vasc Res

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The histopathology of chronic pulmonary hypertension includes microvascular proliferation and neointimal formation. Nitric oxide (NO) has been implicated in the regulation of these mechanisms, but how NO controls microvascular proliferation and its effect on pulmonary microvascular cells is still unclear. In this study, we characterized the in vitro effects of NO on rat pulmonary microvascular smooth muscle cell (PMVSMC) proliferation and investigated the contribution of the p42/44 mitogen-activated protein kinase (MAPK) pathway and p21^waf1/cip1 induction to this response. NO donors inhibited PMVSMC proliferation in a dose-dependent manner. In the presence of hypoxia, the degree of inhibition was significantly enhanced. This inhibition was reversible and independent of apoptosis. The soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) had no impact on proliferation rates, suggesting a cyclic guanosine monophosphate-independent process. Administration of MEK1/2 inhibitors failed to abrogate the antimitotic effect of NO. There was a two- fold induction of the cyclin-dependent kinase inhibitor p21 in PMVSMC treated with NO donors. Under hypoxic conditions, NO caused a three-fold increase in p21 levels. These results demonstrate that NO inhibits PMVSMC proliferation and that this inhibition is not the result of p42/44 MAPK activation. The ability of NO to induce p21 upregulation may be a mechanism by which it exerts antiproliferative effects in PMVSMC.

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“…NO has been associated with several intracellular signaling cascades [10, 11, 12, 13]. One such family of signaling proteins is the MAPKs.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Exogenous Nitric Oxide Upregulates p21<sup>waf1/cip1</sup> in Pulmonary Microvascular Smooth Muscle Cells

Stotz

Johns³

2004

J Vasc Res

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“…The activated sGC increases the levels of cGMP which increases its downstream effects via PKG. In glomeruli, protein kinase G (PKG) is present in smooth muscle and mesangial cells [ 92 ]. Heterogeneous distribution of eNOS and sGC and uniform distribution of sGC and PKG suggests that NO acts through elevation of cGMP, a second messenger of the G-protein pathway.…”

Section: Interaction With Alpha Adrenergic Receptors Of the Kidneymentioning

confidence: 99%

Role of Nitric Oxide in the Cardiovascular and Renal Systems

Asghari

Dempsey

Daneva

et al. 2018

IJMS

205

122

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The gasotransmitters are a family of gaseous signaling molecules which are produced endogenously and act at specific receptors to play imperative roles in physiologic and pathophysiologic processes. As a well-known gasotransmitter along with hydrogen sulfide and carbon monoxide, nitric oxide (NO) has earned repute as a potent vasodilator also known as endothelium-derived vasorelaxant factor (EDRF). NO has been studied in greater detail, from its synthesis and mechanism of action to its physiologic, pathologic, and pharmacologic roles in different disease states. Different animal models have been applied to investigate the beneficial effects of NO as an antihypertensive, renoprotective, and antihypertrophic agent. NO and its interaction with different systems like the renin–angiotensin system, sympathetic nervous system, and other gaseous transmitters like hydrogen sulfide are also well studied. However, links that appear to exist between the endocannabinoid (EC) and NO systems remain to be fully explored. Experimental approaches using modulators of its synthesis including substrate, donors, and inhibitors of the synthesis of NO will be useful for establishing the relationship between the NO and EC systems in the cardiovascular and renal systems. Being a potent vasodilator, NO may be unique among therapeutic options for management of hypertension and resulting renal disease and left ventricular hypertrophy. Inclusion of NO modulators in clinical practice may be useful not only as curatives for particular diseases but also for arresting disease prognoses through its interactions with other systems.

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Extended Abstracts of Invited Lectures

Cited by 2 publications

References 1 publication

Exogenous Nitric Oxide Upregulates p21<sup>waf1/cip1</sup> in Pulmonary Microvascular Smooth Muscle Cells

Exogenous Nitric Oxide Upregulates p21<sup>waf1/cip1</sup> in Pulmonary Microvascular Smooth Muscle Cells

Role of Nitric Oxide in the Cardiovascular and Renal Systems

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