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Abstract

Our objective was to determine whether subarachnoid haemorrhage modifies cerebral artery smooth muscle cell phenotype and the contractile protein alpha-actin measured 7 days after haemorrhage. We used a rabbit subarachnoid haemorrhage model and immunofluorescence labelling of alpha-smooth muscle actin, vimentin and desmin. The paired comparison between the haemorrhage and sham rabbits was performed using confocal laser-scanning microscopy. We found in the haemorrhage group significantly less intense alpha-actin immunostaining (p = 0.036) and more intense vimentin immunostaining (p = 0.043) but no significant change in the intensity of desmin staining. Our results indicate an absolute decrease after subarachnoid haemorrhage in the amount of functional alpha-actin and in the light of the literature may suggest a certain degree of dedifferentiation of smooth muscle cells in the cerebral artery wall.

Intracranial Hemorrhage: Mechanisms of Secondary Brain Injury

“…This type of denervation could be expected to result in loss of neurogenic control of cerebral arteries [55] and impairment of autoregulation. In the media, myonecrosis occurs with loss of contractile protein in the smooth muscle [58, 59]; additionally, the amount of interstitial collagen increases [58]. Together these processes contribute to arterial narrowing which is not vasospasm-mediated [60].…”

Imatinib attenuates cerebrovascular injury and phenotypic transformation after intracerebral hemorrhage in rats

“…As early as 1997, however, evidence began to accumulate indicating that the blood-brain barrier, and possibly small arteries, were also injured by ICH (4). Further evidence demonstrated that intracerebral blood could alter cytoskeletal organization within cerebral arteries (17) and even induce contractile dedifferentiation (36). Current evidence strongly implies that phenotypic transformation of cerebrovascular smooth muscle and altered contractile function are prominent consequences of ICH (42,52), although the mechanisms mediating this vascular injury remain unclear.…”

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

“…Vascular remodeling after SAH, as well as cellular growth, could be mainly attributed to increased beta-actin mRNA expression [ 543 ]. The decreased alpha-actin intensity in VSMC probably contributes to the VSMC shift towards a more synthetic (less differentiated) phenotype [ 544 ].…”