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J Thorac Cardiovasc Surg 2006;131:138-145
© 2006 The American Association for Thoracic Surgery

Evolving Technology

An Egr-1 master switch for arteriogenesis: Studies in Egr-1 homozygous negative and wild-type animals

Cristian Sorin Sarateanu, MD a , Mauricio A. Retuerto, BS a , James T. Beckmann, BS a , Leslie McGregor, BS a , JoAnn Carbray, BS a , Gerald Patejunas, PhD b , Lina Nayak a , Jeffrey Milbrandt, MD c , Todd K. Rosengart, MD b , *

a Evanston Northwestern Healthcare, Evanston, Ill
b Evanston Northwestern Healthcare, Evanston, Ill, and Feinberg School of Medicine of Northwestern University, Chicago, Ill
c Washington University, St Louis, Mo

Received for publication April 11, 2005; revisions received July 12, 2005; accepted for publication August 2, 2005.

* Address for reprints: Todd K. Rosengart, MD, 2650 Ridge Ave, Burch 100, Evanston, IL 60201 (Email: trosengart{at}enh.org).

BACKGROUND: Arteriogenesis has been implicated as an important biologic response to acute vascular occlusion. The early growth response 1 (Egr-1) gene encodes an immediate-early response transcription factor that is upregulated by changes in vascular strain and that in turn upregulates a number of putative angiogenic and arteriogenic growth factors. We therefore hypothesized that early growth response 1 might be a critical arteriogenic messenger that induces revascularization in the setting of acute vascular occlusions.

METHODS: Wild-type or Egr-1–/– (null) C57 BL mice, or Sprague-Dawley rats, underwent unilateral iliofemoral artery excision and subsequent analyses for angiogenesis and arteriogenesis through cell-specific immunohistochemistry. Rats were also administered an adenoviral vector encoding for Egr-1 (AdEgr group), noncoding vectors (AdNull group), or saline, after which these animals were assessed by means of serial laser Doppler perfusion imaging and morphologic examination of rat foot-pad ischemic lesions.

RESULTS: Egr-1 wild-type mice demonstrated an equivalent number of capillaries but a greater number of arterioles following excision versus Egr-1 null mice. AdEgr group rats demonstrated greater distal perfusion from 7 to 21 days after excision compared with control animals (P < .02), which approximated normal perfusion at 21 days after excision. AdEgr group rats also demonstrated greater arteriolar density and less severe ischemic foot-pad lesions than control animals.

CONCLUSION: These data suggest the importance of Egr-1 as a critical and potentially therapeutic mediator of revascularization after vascular occlusion and implicate arteriogenesis (collateral vessel formation) as a critical component of this process.

Abbreviations and Acronyms AdEgr-1 = adenoviral vector encoding for Egr-1; AdNull = noncoding vector; Egr-1 = early growth response transcription factor 1; LDPI = laser Doppler perfusion imaging; PBS = phosphate-buffered saline; ROI = region of interest; SMA = smooth muscle actin; VEGF = vascular endothelial growth factor






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