Laboratory: Cerebrovascular Dysfunctions

PREVIOUS PROJECTS

Cytoskeletal Proteins in normal and pathological conditions (Constantinescu E. et al., Cell Biol Internatl Rep, 1986; Heltianu C. et al., Rev Roum Biochim, 1986; Constantinescu E. et al., J Submicrosc Cytol Pathol 1997)

Cellular events in atherogenesis (Constantinescu E. et al., J Submicrosc Cytol Pathol, 2000; Constantinescu E. et al., J Submicr Cytol Pathol, 2002; Rus HG.et al., Atherosclerosis 1986)

Alteration of the cerebral microvasculature during aging (Safciuc F. et al., Current Neurovasc Res, 2007; Constantinescu E. et al., Current Neurovasc Res, 2011)
Inhibition of gelatinase activity in atherosclerosis and diabetes (Nicolae M. et al., J Cell Mol Med 2005; Sváb I. et al., J Cell Mol Med 2004).

CURRENT PROJECT

Fig. 1. Amyloid specific staining of paraffin kidney sections from HL hamsters.
a) Hematoxylin staining showing areas with glomeruli (G); b) Congo red staining, examined in bright field, shows the pink signal on glomeruli; c) Congo red staining, examined in fluorescence, displays a strong red signal; d) Thioflavin S staining, examined in fluorescence, labels the glomeruli and the proximal tubules (T); e) Detailed labeling of glomeruli and proximal tubules; and a marked staining of the Bowman capsule (inset, B); f) Thioflavin S staining of normal kidney section show no specific labeling.

The correlation between the hyperlipidemic diet and amyloidoses

Aim. Amyloidoses are clinical disorders in which misfolded proteins accumulate extracellularly in tissues as insoluble fibrils, impairing the normal organ function. The correlation between hyperlipidemia and localized amyloidoses is not well documented so far. The aim of the present study is to determine if the hyperlipemic (HL) diet causes amyloid accumulation.

In the atherosclerotic process the kidney, liver, pancreas and small intestine represent target organs affected by this disease. Our hypothesis was that beside the hyperlipidemia-induced affliction of the mentioned organs microcirculation, amyloid deposition could be an aggravating cause for their malfunction.

Results: The experiments were performed on Golden Syrian hamsters fed either standard diet or HL diet for up to 9 months, when serum cholesterol and triglycerides levels were significantly increased in HL hamsters compared to control animals.

Sections of kidney, small intestine, liver and pancreas stained with Congo red and thioflavin S for specific detection of amyloid revealed that all organs display significant amyloid deposits compared to normal hamster’s organs.

Our results revealed so far that HL diet may induce the formation of localized amyloid deposits in kidney, small intestine, liver and pancreas. The study could bring another medical warning about the risks of the HL diet that induces pathogenic consequences, not only in cardiovascular diseases but also in the development of localized amyloidoses.