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American Journal of Pathology, Vol 146, 56-66, Copyright © 1995 by American Society for Investigative Pathology

REGULAR ARTICLES

Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar

A Desmouliere, M Redard, I Darby and G Gabbiani
Department of Pathology, University of Geneva, Switzerland.

Granulation tissue formation and contraction is an important step of second intention wound healing. Granulation tissue develops from the connective tissue surrounding the damaged or missing area and its cellular components are mainly small vessel and inflammatory cells as well as fibroblasts and myofibroblasts. As the wound closes and evolves into a scar, there is an important decrease in cellularity; in particular myofibroblasts disappear. The question arises as to which process is responsible for this cellular loss. During a previous investigation on the expression of alpha-smooth muscle actin in myofibroblasts (Darby I, Skalli O, Gabbiani G, Lab Invest, 1990, 63:21- 29), we have observed that in late phases of wound healing, many myofibroblasts show changes compatible with apoptosis and suggested that this type of cell death could be responsible for the disappearance of myofibroblasts. We have now tested this hypothesis by means of morphometry at the electron microscopic level and by in situ end labeling of fragmented DNA. Our results indicate that the number of myofibroblastic and vascular cells undergoing apoptosis increases as the wound closes and support the assumption that this is the mechanism of granulation tissue evolution into a scar. The regulation of apoptotic phenomena during wound healing may be important in scar establishment and development of pathological scarring.

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				A. J. Singer and R. A.F. Clark Cutaneous Wound Healing N. Engl. J. Med., September 2, 1999; 341(10): 738 - 746. [Full Text] [PDF]

				N. Funato, K. Moriyama, Y. Baba, and T. Kuroda Evidence for Apoptosis Induction in Myofibroblasts during Palatal Mucoperiosteal Repair Journal of Dental Research, September 1, 1999; 78(9): 1511 - 1517. [Abstract] [PDF]

				Y. Hayakawa, G. Takemura, J. Misao, M. Kanoh, M. Ohno, H. Ohashi, H. Takatsu, H. Ito, K. Fukuda, T. Fujiwara, et al. Apoptosis and Overexpression of Bax Protein and bax mRNA in Smooth Muscle Cells Within Intimal Hyperplasia of Human Radial Arteries : Analysis With Arteriovenous Fistulas Used for Hemodialysis Arterioscler Thromb Vasc Biol, September 1, 1999; 19(9): 2066 - 2077. [Abstract] [Full Text] [PDF]

				H. Sugiyama, J. S. Savill, M. Kitamura, L. Zhao, and E. Stylianou Selective Sensitization to Tumor Necrosis Factor-alpha -induced Apoptosis by Blockade of NF-kappa B in Primary Glomerular Mesangial Cells J. Biol. Chem., July 9, 1999; 274(28): 19532 - 19537. [Abstract] [Full Text] [PDF]

				D. W. Powell, R. C. Mifflin, J. D. Valentich, S. E. Crowe, J. I. Saada, and A. B. West Myofibroblasts. I. Paracrine cells important in health and disease Am J Physiol Cell Physiol, July 1, 1999; 277(1): C1 - C19. [Abstract] [Full Text] [PDF]

				K. Pels, M. Labinaz, C. Hoffert, and E. R. O'Brien Adventitial Angiogenesis Early After Coronary Angioplasty : Correlation With Arterial Remodeling Arterioscler Thromb Vasc Biol, February 1, 1999; 19(2): 229 - 238. [Abstract] [Full Text] [PDF]

				A. TAN, H. LEVREY, C. DAHM, V. A. POLUNOVSKY, J. RUBINS, and P. B. BITTERMAN Lovastatin Induces Fibroblast Apoptosis In Vitro and In Vivo . A Possible Therapy for Fibroproliferative Disorders Am. J. Respir. Crit. Care Med., January 1, 1999; 159(1): 220 - 227. [Abstract] [Full Text]

				N. Hussain, F. Wu, L. Zhu, R. S. Thrall, and M. J. Kresch Neutrophil Apoptosis during the Development and Resolution of Oleic Acid-Induced Acute Lung Injury in the Rat Am. J. Respir. Cell Mol. Biol., December 1, 1998; 19(6): 867 - 874. [Abstract] [Full Text]

				L. A. Ortiz, K. Moroz, J.-Y. Liu, G. W. Hoyle, T. Hammond, R. F. Hamilton, A. Holian, W. Banks, A. R. Brody, and M. Friedman Alveolar macrophage apoptosis and TNF-alpha , but not p53, expression correlate with murine response to bleomycin Am J Physiol Lung Cell Mol Physiol, December 1, 1998; 275(6): L1208 - L1218. [Abstract] [Full Text] [PDF]

				B. D. Uhal, C. Ramos, I. Joshi, A. Bifero, A. Pardo, and M. Selman Cell size, cell cycle, and alpha -smooth muscle actin expression by primary human lung fibroblasts Am J Physiol Lung Cell Mol Physiol, November 1, 1998; 275(5): L998 - L1005. [Abstract] [Full Text] [PDF]

				G. Bauriedel, S. Schluckebier, R. Hutter, U. Welsch, R. Kandolf, B. Luderitz, and M. F. Prescott Apoptosis in Restenosis Versus Stable-Angina Atherosclerosis : Implications for the Pathogenesis of Restenosis Arterioscler Thromb Vasc Biol, July 1, 1998; 18(7): 1132 - 1139. [Abstract] [Full Text] [PDF]

				G. Takemura, M. Ohno, Y. Hayakawa, J. Misao, M. Kanoh, A. Ohno, Y. Uno, S. Minatoguchi, T. Fujiwara, and H. Fujiwara Role of Apoptosis in the Disappearance of Infiltrated and Proliferated Interstitial Cells After Myocardial Infarction Circ. Res., June 15, 1998; 82(11): 1130 - 1138. [Abstract] [Full Text] [PDF]

				J. C. Schittny, V. Djonov, A. Fine, and P. H. Burri Programmed Cell Death Contributes to Postnatal Lung Development Am. J. Respir. Cell Mol. Biol., June 1, 1998; 18(6): 786 - 793. [Abstract] [Full Text]