Dr. Enrico Stefani
High Resolution Confocal Microscopy
in the Cardiovascular System
BH-520 CHS
310- 794 -7804
estefani@ucla.edu
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Research Interests:

The main goals on my laboratory is TO VISUALIZE STATIC AND DYNAMIC CHANGES OF MACROMOLECULAR COMPLEXES REGULATING HEART AND VASCULAR SIGNALING IN A PRESSURE OVERLOAD MODEL OF HEART FAILURE. To this end we are developing and building “Nanomicroscopes” for fluorescence imaging allowing the measurement of structures and their dynamics inside a cell with a 3D spatial resolution down to the scale of 20-40 nm while maintaining the microscopic scale over a 20-100 µm range. My research is driven by this need and it will facilitate the mapping of macromolecular complexes remodeling in a pressure-overload model of cardiovascular disease.

Representative Publications:

M. Eghbali, R. Deva, A. Alioua, Tamara Y. Minosyan, Hongmei Ruan, Y. Wang, L. Toro and Enrico Stefani.  (2005)
Molecular and Functional Signature of Heart Hypertrophy in Mice during Pregnancy. Circulation Research 96(11):1208-16.

Ropero A., Eghbali M., Minosyan, T.Y., Tang, G., Toro L. and Enrico Stefani. (2006)
Heart Estrogen Receptor Alpha: Distinct Membrane and Nuclear Distribution Patterns and Regulation by Estrogen. Journal of Molecular and Cellular Cardiology 41:496-510.

Eghbali M., Wang Y., Toro L., and Enrico Stefani. (2006)
Heart hypertrophy during pregnancy: a better functioning heart? Trends Cardiovasc Med. 16(8):285-91.

The figure illustrates remodeling of α1C channel and ryanodine (RyR) receptors in ventricular cardiomyocytes by pressure overload. (Aa-Cc; Gg-Ii) Deconvolved single confocal planes of cardiomyocytes immunostained with anti-α1C (green) and anti-RyR (red) Ab from a control mouse (Aa-Cc) and from a mouse undergoing pressure overload 3 weeks after TAC (Gg-Ii). (a-c, g-i) Corresponding regions marked with squares in (A-C; G-I) at higher display amplification. The organized pattern of α1C and RyR is lost in the failing heart where there is a lower degree of association between α1C and RyR (Gg-Ii). Note the smaller α1C cluster size when comparing control (a) with pressure overload (g). The degree of association between of α1C and RyR was quantified by measuring PPI in control (D,E) and in pressure overload (J,K). (D,J;E,K) Correlation coefficient (CC) histograms and P sign value vs. CC plot. PPI decreased from 0.43 in control to 0.14 in pressure overload. (F,L) Reduction of PPI as function of the shift of one plane in the x axis validating the association between α1C and RyR.

CONTROL

FAILING HEART