α<sub>2D/A</sub>‐adrenergic receptor gene induction in the retina by phorbol ester: involvement of an AP‐2 element

Venkataraman, V.; Duda, Teresa; Sharma, Rameshwar K.

doi:10.1046/j.1365-2443.1999.00249.x

Cited by 3 publications

(1 citation statement)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Alcohol is a known activator of PKC in various cell types[32–35] and PKC has been implicated in the induction of the α 2A -AR gene transcription [36, 37]. As reported by Venkataraman et al ., [37] the increase in α 2A -AR mRNA resulting from the exposure of rat C6 glioma cells to phorbol- 12, 13-myristate acetate (PMA) was mediated by PKC through the AP-2 element of the α 2A -AR promoter. PMA, like alcohol, is an activator of PKC [38, 39].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Ajakaiye¹,

Jacob²,

Wu³

et al. 2011

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

Alcohol-induced liver disease is associated with unacceptable morbidity and mortality. When activated, Kupffer cells (KCs), the resident macrophages in the liver, release proinflammatory cytokine TNF-α, a key mediator of hepatic damage. Although chronic alcohol causes increase in norepinephrine (NE) release leading to hepatic dysfunction, the mechanism of NE-induced hepatic injury in chronic alcohol exposure has not been elucidated. This study was conducted to determine whether chronic alcohol exposure increases NE and upregulates KC α2A-adrenoceptors (α2A-AR) to cause TNF-α release. We also examined the role of mitogen activated protein kinase (MAPK) phosphatase-1 (MKP-1) in this process. Male adult rats were fed the Lieber-DeCarli liquid diet containing alcohol as 36% of total calories. The animals were sacrificed after 6 weeks and blood and liver samples were harvested for further analysis. KCs from healthy male rats were cultured with alcohol for 7 days, and cells then harvested for RNA and protein analyses. Chronic alcohol exposure resulted in hepatic damage. Alcohol caused a 276% increase in circulating NE and 86% increase in TNF-α in the liver. There was a 75% and 62% decrease in MKP-1 mRNA and protein levels in the liver, respectively. In-vitro experiments revealed 121% and 98% increase in TNF-α and α2A-AR mRNA levels with alcohol exposure, respectively, and a 32% decrease in MKP-1 mRNA compared to controls. In summary, chronic alcohol exposure elevates NE and upregulates KC α2A-AR to release TNF-α. Alcohol induced downregulation of MKP-1 leads to further release of TNF-α and hepatic injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Ajakaiye¹,

Jacob²,

Wu³

et al. 2011

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

show abstract

Membrane guanylate cyclase is a beautiful signal transduction machine: overview

Sharma

2009

Mol Cell Biochem

104

View full text Add to dashboard Cite

This article is a sequel to the four earlier comprehensive reviews which covered the field of membrane guanylate cyclase from its origin to the year 2002 (Sharma in Mol Cell Biochem 230:3-30, 2002) and then to the year 2004 (Duda et al. in Peptides 26:969-984, 2005); and of the Ca(2+)-modulated membrane guanylate cyclase to the year 1997 (Pugh et al. in Biosci Rep 17:429-473, 1997) and then to 2004 (Sharma et al. in Curr Top Biochem Res 6:111-144, 2004). This article contains three parts. The first part is "Historical"; it is brief, general, and freely borrowed from the earlier reviews, covering the field from its origin to the year 2004 (Sharma in Mol Cell Biochem, 230:3-30, 2002; Duda et al. in Peptides 26:969-984, 2005). The second part focuses on the "Ca(2+)-modulated ROS-GC membrane guanylate cyclase subfamily". It is divided into two sections. Section "Historical" and covers the area from its inception to the year 2004. It is also freely borrowed from an earlier review (Sharma et al. in Curr Top Biochem Res 6:111-144, 2004). Section "Ca(2+)-modulated ROS-GC membrane guanylate cyclase subfamily" covers the area from the year 2004 to May 2009. The objective is to focus on the chronological development, recognize major contributions of the original investigators, correct misplaced facts, and project on the future trend of the field of mammalian membrane guanylate cyclase. The third portion covers the present status and concludes with future directions in the field.

show abstract

Alpha-2A Adrenoceptor

Bylund

2007

xPharm: The Comprehensive Pharmacology Reference

View full text Add to dashboard Cite

α_2D/A‐adrenergic receptor gene induction in the retina by phorbol ester: involvement of an AP‐2 element

Cited by 3 publications

References 43 publications

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Membrane guanylate cyclase is a beautiful signal transduction machine: overview

Alpha-2A Adrenoceptor

Contact Info

Product

Resources

About

α2D/A‐adrenergic receptor gene induction in the retina by phorbol ester: involvement of an AP‐2 element

Cited by 3 publications

References 43 publications

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Upregulation of Kupffer cell α2A-Adrenoceptors and downregulation of MKP-1 mediate hepatic injury in chronic alcohol exposure

Membrane guanylate cyclase is a beautiful signal transduction machine: overview

Alpha-2A Adrenoceptor

Contact Info

Product

Resources

About

α_2D/A‐adrenergic receptor gene induction in the retina by phorbol ester: involvement of an AP‐2 element