Disease relevance of Plin

• Penumbral alkalosis appeared to be a time-dependent event occurring 30 to 60 minutes after the passage of peri-infarct depolarizations [1].
• Thus, reperfusion causes damage to the tissue at the focus of ischemia while triggering remodeling in the peri-infarct region by means of perceived hyperoxia [2].
• MI+RWJ also demonstrated increased myocyte hypertrophy in the peri-infarct and non-infarct zones, and reduced myocardial collagen and alpha-smooth muscle actin (SMA) immunoreactivity compared with MI+V [3].
• Factors influencing the frequency of fluorescence transients as markers of peri-infarct depolarizations in focal cerebral ischemia [4].
• Hyperglycemia delays terminal depolarization and enhances repolarization after peri-infarct spreading depression as measured by serial diffusion MR mapping [5].

Psychiatry related information on Plin

• It has been suggested that pre-natal and or peri-natal hypoxia can cause permanent hearing loss as a result of interference with the generation of the endocochlear potential, especially if this interference occurs during the critical period of endocochlear potential development [6].

High impact information on Plin

• The neoangiogenesis resulted in decreased apoptosis of hypertrophied myocytes in the peri-infarct region, long-term salvage and survival of viable myocardium, reduction in collagen deposition and sustained improvement in cardiac function [7].
• Expression of this cytokine is not only confined strictly to the infarct or peri-infarct zone but is expressed by cardiac myocytes within the myocardium contralateral to the infarct [8].
• The major cAMP-dependent protein kinase (A-kinase) substrate in adipocytes is perilipin, a protein found exclusively at the surface of the lipid storage droplets [9].
• However, in either the presence or the absence of agonists, A-kinase was activated as assessed by examining the phosphorylation of the major adipocyte A-kinase substrate, perilipin [10].
• This increase in expression was limited to the immediate peri-infarct region and was absent from remote areas of the left or right ventricles [11].

Chemical compound and disease context of Plin

• The results also suggest that the relationship of frequency of peri-infarct depolarizations with plasma glucose requires further examination, to confirm the finding and to determine a safe lower limit for a target range for control of plasma glucose if insulin is used in the management of patients with cerebral ischemia [4].
• In the peri-infarct cortex, irbesartan treatment decreased the number of apoptotic cells on day 3 and attenuated the invasion of activated microg-lia and macrophages on days 3 and 7 after ischemia [12].
• The current study tested whether peri-neural clonidine at the time of injury could also prevent development of hypersensitivity [13].
• Reduction of proteinuria in rats treated with enalapril and losartan was associated with a reduction in Ang II levels in both the peri-infarct and intact portions of the remnant kidney [14].
• CONCLUSIONS: Peri-infarct renal tissue Ang II levels and plasma Ang II and aldosterone levels increase transiently during the evolution of hypertension in the remnant kidney model [15].

Biological context of Plin

• The predicted perilipin A contains peptides present in proteolytic digests of the purified 62-kDa form of perilipin from rat adipocytes, as well as the requisite consensus A-kinase phosphorylation sites [9].
• Chronic ethanol feeding also decreased beta-adrenergic receptor-stimulated protein kinase A activation and phosphorylation of its downstream proteins, perilipin A and hormone-sensitive lipase, the primary lipase-mediating lipolysis [16].
• Immunocytochemistry with antibodies raised against the intracellular C-terminus of the P2X7 receptor showed a time-dependent upregulation of labeled cells in the peri-infarct region after right middle cerebral artery occlusion (MCAO) in comparison to controls [17].
• Hippocampal long-term potentiation (LTP) is reduced in aged relative to young F-344 rats when peri-threshold stimulation protocols (several stimulus pulses at 100-200 Hz) are used [18].
• In order to identify biological processes relevant for cell death and survival in the brain following stroke, the postischemic brain transcriptome was studied by a large-scale cDNA array analysis of three peri-infarct brain regions at eight time points during the first 24 h of reperfusion following middle cerebral artery occlusion in the rat [19].

Anatomical context of Plin

• Isolation of cDNAs for perilipins A and B: sequence and expression of lipid droplet-associated proteins of adipocytes [9].
• Perilipin, a member of this family, is expressed exclusively in the adipose tissue and regulates the breakdown of triacylglycerol in LDs via its phosphorylation [20].
• Under basal conditions, HSL resided predominantly in the cytosol and unphosphorylated perilipin upon the lipid droplet [21].
• Ang-2 mRNA was up-regulated 6 hours after MCAO and was mainly observed in endothelial cell (EC) cord tips in the peri-infarct and infarct area [22].
• This protein, which we term perilipin, is found in differentiated cultured 3T3-L1 adipocytes, but not in their precursor 3T3-L1 fibroblasts [23].

Associations of Plin with chemical compounds

• An increasing number of proteins have been reported to be associated with intracellular triglyceride (TG), among them the PAT family members: perilipin, ADRP (for adipocyte differentiation-related protein), and TIP47 (for tail-interacting protein of 47 kDa) [24].
• Upon lipolytic stimulation of adipocytes isolated from young rats with the beta-adrenergic agonist, isoproterenol, HSL translocated from the cytosol to the lipid droplet, but there was no movement of perilipin from the droplet to the cytosol; however, perilipin phosphorylation was observed [21].
• We report that in intact primary adipocytes exogenous oleic acid was taken up and directly converted to TG in the plasma membrane, in a novel subclass of caveolae that specifically contains the protein perilipin [25].
• The cortical infarct volume was larger in the early training group than in the other two groups (P < .005), possibly related to increased glutamate release and peri-infarct cortical hyperexcitability [26].
• The present study was performed to determine the spatial and temporal expression of osteopontin and its integrin receptor alpha(v)beta3 during formation of the peri-infarct gliotic barrier and subsequent formation of a new glial-limiting membrane [27].

Other interactions of Plin

• The aim of the present study was to investigate the effect of PKA and PKC activities on the distribution of perilipin and ADRP in primary cultured adrenal cells, and the role of ERK in PMA- and calphostin C-induced steroidogenesis [28].

Analytical, diagnostic and therapeutic context of Plin

• Moreover, specific immunofluorescence became evident at cell surfaces and in peri- and supranuclear localization, sites essentially negative in the controls [29].
• Adipocyte lipolysis was compared with hormone-sensitive lipase (HSL)/perilipin subcellular distribution and perilipin phosphorylation using Western blot analysis [21].
• To assess the role of gut-derived endotoxaemia and endogenous cytokines in these changes, the effects of peri-operative treatment with either the lipopolysaccharide-neutralizing bactericidal/permeability-increasing protein or interleukin-1 receptor antagonist were investigated at 24 h after two-thirds hepatectomy in rats [30].
• Noninvasive near infrared spectroscopy monitoring of regional cerebral blood oxygenation changes during peri-infarct depolarizations in focal cerebral ischemia in the rat [31].
• Increases in perfusion pressure were produced by peri-arterial electrical stimulation of the mesenteric sympathetic nerves at 3, 6 and 10 Hz before and after the intravenous administration of frusemide 5 mg/kg [32].

References