Serum Heat Shock Protein 90 Alpha: A New Marker of Hypertension-Induced Endothelial Injury?

Abstract

substances, including NO, prostaglandins (PGI2 and PGE2), and a family of endothelial-derived hyperpolarizing factors (EDHF), such as hydrogen sulfide, hydrogen peroxide, potassium ions, carbon monoxide, epoxyeicosatrienoic acids, and C-natriuretic peptide, which activate potassium channels of the vascular smooth muscle cells [2].Arterial hypertension is associated with an impaired function of nitric oxide [1,2]. This gaseous lipophilic free radical is generated by three isoforms Arterial hypertension, as one of the most prevalent causes of cardiovascular events, is a widespread public health problem. The disorder results from an endothelial dysfunction associated with an impaired bioavailability of nitric oxide (NO), which is known to be one of the crucial factors for maintenance of normal blood pressure. Essential hypertension is linked to reduced endothelium--dependent vessel relaxation [1,2]. Normal vasorelaxation is mediated by a number of endothelial Objectives. The objective of the study was to evaluate serum concentrations of Hsp-90a in patients with arterial hypertension in comparison to their normotensive counterparts. Material and Methods. The study was performed on 49 adults (mean age 55.6 years) with an elevated waist circumference. The individuals presented no subjective feeling of any disease, admitted no drug treatment for any condition, and had not previously been diagnosed with the metabolic syndrome. Patients were screened for arterial hypertension and other component disorders of the metabolic syndrome. Hsp-90a concentrations were evaluated by enzyme-linked immunosorbent assay (ELISA). Results. Twenty-eight subjects were diagnosed with arterial hypertension, while 21 individuals had normal blood pressure. Twenty-five patients satisfied the metabolic syndrome diagnostic criteria. Hsp-90a concentrations were significantly higher (p = 0.002) in the individuals with arterial hypertension than in their normotensive counterparts (median ± interquartile range): 19.42 ng/mL ± 5.17 vs. 16.86 ng/mL ± 3.18. The concentrations of Hsp-90a correlated positively with systolic blood pressure (R = 0.39; p = 0.005) and diastolic blood pressure (R = 0.29; p = 0.046).Conclusions. An increase in Hsp-90a concentrations in patients with arterial hypertension may be a compensatory mechanism for the impaired bioavailability of nitric oxide. The role of Hsp-90a as an early marker of hypertension-associated endothelial injury should be confirmed in further studies on a larger group of patients (Adv Clin Exp Med 2015, 25, 2, 255-261).

The Role of HSP90 Inhibitors in the Treatment of Cardiovascular Diseases

“…Hypertension-induced endothelial dysfunction is associated with impaired nitric oxide (NO) bioavailability regulated through the interaction between nitric oxide synthase and HSPs [ 67 ]. It is well known that nitric oxide is one of the key factors in maintaining normal blood pressure.…”

“…Interestingly, all isoforms of NOS (neuronal (nNOS), inducible (iNOS) and eNOS) were initially down-regulated but were eventually significantly increased in the left ventricle of spontaneously hypertensive rats. Increased expression of HSP90α compensates for impaired eNOS function associated with reduced nitric oxide bioavailability [ 67 ]. Increased HSP90α concentrations in patients with arterial hypertension may be a compensatory mechanism for impaired nitric oxide bioavailability [ 67 ], confirming that HSP90α can serve as an early marker of hypertension-related endothelial injury [ 67 ].…”

“…Increased expression of HSP90α compensates for impaired eNOS function associated with reduced nitric oxide bioavailability [ 67 ]. Increased HSP90α concentrations in patients with arterial hypertension may be a compensatory mechanism for impaired nitric oxide bioavailability [ 67 ], confirming that HSP90α can serve as an early marker of hypertension-related endothelial injury [ 67 ]. In addition, it was also found that this study mainly focused on HSP90 in serum.…”

Exploration of the anti-insomnia mechanism of Ganoderma by central-peripheral multi-level interaction network analysis

“…The proinflammatory cytokine TNF increases non-rapid eye movement sleep [29]. HSP90αA1 participates in cell cycle regulation and signal transduction; it also mediates inflammatory responses and apoptosis [44]. CASP3, JUN, and other core proteins are closely related to apoptosis, which may involve TNF [45], although the underlying mechanism is unclear.…”

The Role of Extracellular Heat Shock Proteins in Cardiovascular Diseases

“…In arterial hypertension, elevated levels of HSP90α have been detected. This is thought to be a compensatory mechanism for reduced nitric oxide bioavailability [ 73 ]. Therefore, HSP90α may be an early marker of endothelial injury in hypertensive individuals.…”