RGD Reference Report - Protective role of a novel erythrocyte-derived depressing factor on blood vessels of renovascular hypertensive rats. - Rat Genome Database

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Protective role of a novel erythrocyte-derived depressing factor on blood vessels of renovascular hypertensive rats.

Authors: Pang, H  Wen, YY  Ma, N  Wang, YT  Shi, L 
Citation: Pang H, etal., Clin Exp Pharmacol Physiol. 2007 May-Jun;34(5-6):393-8.
RGD ID: 2289672
Pubmed: PMID:17439406   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1440-1681.2007.04561.x   (Journal Full-text)

1. We have isolated a novel human erythrocyte-derived depressing factor (EDDF) that has a significant antihypertensive effect in various rat models of hypertension. The aim of the present study was to examine the mechanisms of action of EDDF on vascular function in two-kidney, one-clip (2K1C) renovascular hypertensive rats. 2. The EDDF was prepared from human erythrocytes. Experiments were performed in 18 male Wistar rats. The vascular ring perfusion assay and a two-photon laser scanning fluorescence microscope (TMP) were used to evaluate the vascular contractile response. The effects of EDDF on phenylephrine (PE)- and noradrenaline (NA)-induced vascular contraction were evaluated in 2K1C hypertensive rats. The proliferation and DNA synthesis in vascular smooth muscle cells (VSMC) were determined using the [3H]-TdR (thymidine) incorporation and 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assays. Flow cytometry, reverse transcription-polymerase chain reaction and western blots were used to measure cell cycle and apoptotic profiles, platelet-derived growth factor (PDGF)-A expression and the activity of extracellular signal-regulated kinase (ERK)-1/2, as well as the expression of cyclin D1 and cyclin-dependent kinase (CDK) 4. 3. At 10(-5) g/mL, EDDF significantly decreased the PE- and NA-induced hypertensive vascular contraction. In addition, EDDF inhibited DNA synthesis in primary VSMC from 2K1C rats. The mRNA expression of PDGF-A in VSMC was twofold higher in 2K1C rats compared with control rats, whereas EDDF significantly inhibited the increment in PDGF-A mRNA expression. In addition, EDDF inhibited the phosphorylation of ERK1/2 and decreased the expression of cyclin D1 and CDK4; p21 (Cip1) levels were increased after treatment with EDDF. 4. In conclusion, EDDF inhibits VSMC proliferation in 2K1C rats through G0/G1 cell cycle arrest. The effects may be mediated, in part, by enhanced expression of p21 (Cip1) and the inhibition of ERK1/2 phosphorylation and the expression of cyclin D1/CDK4 and PDGF-A.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
renal hypertension  ISOCdkn1a (Rattus norvegicus)2289672; 2289672protein:decreased expression:vascular associated smooth muscle cellRGD 
renal hypertension  IEP 2289672protein:decreased expression:vascular associated smooth muscle cellRGD 
renovascular hypertension  ISOPdgfa (Rattus norvegicus)2289672; 2289672mRNA:increased expression:vascular associated smooth muscle cellRGD 
renovascular hypertension  IEP 2289672mRNA:increased expression:vascular associated smooth muscle cellRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cdkn1a  (cyclin-dependent kinase inhibitor 1A)
Pdgfa  (platelet derived growth factor subunit A)

Genes (Mus musculus)
Cdkn1a  (cyclin dependent kinase inhibitor 1A)
Pdgfa  (platelet derived growth factor, alpha)

Genes (Homo sapiens)
CDKN1A  (cyclin dependent kinase inhibitor 1A)
PDGFA  (platelet derived growth factor subunit A)


Additional Information