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2010 | 5 | 5 | 556-564
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Apoptosis quantification at the respiratory epithelium level in asthma

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The „changes” occurring in the expression of the factors involved in the apoptotic chain at the level of the respiratory epithelium in asthma is still an unsolved issue. At this level an important role is played by the mitochondria and the factors that influence the membrane permeability, especially the Bcl-2 super family. The purpose of this study is to evaluate both the changes in the expression of the Bcl-2 and of the Bax proapoptotic factors at the respiratory epithelium level in 21 patients with bronchial asthma of different degrees of severity of disease (aaccording to GINA - Global Initiative For Asthma). To accomplish this, fragments of the bronchial mucosa were obtained through fiberbronchoscopy, being afterwords hystologically prepare in view of the immunomarking with anti Bcl-2 and anti-Bax antibodies. Microscopic examination revealed an important decrease in the level of proapoptotic factor Bcl-2 in patients with persistent severe forms of the disease and a significant decrease in the expression of the proapototic Bax factor at the respiratory epithelium level even in the early stages of the disease. Knowing all the factors involved in apoptosis at the respiratory epithelium level in bronchial asthma, as well as of their expression changes will be at the core of new therapeutical approaches to of this disease.
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  • Department of Histology, School of Medicine, “Gr.T.Popa” University of Medicine and Pharmacy, No. 16 Universitatii Street, 700115, Iasi, Romania,
  • Outpatient Department, Clinic of Pulmonary Diseases, No. 30 I. Cihac Street, 700115, Iasi, Romania
  • Department of Pneumology, School of Medicine, “Gr.T.Popa” University of Medicine and Pharmacy, No. 16 Universitatii Street, 700115, Iasi, Romania
  • Department of Allergology and Immunology, School of Medicine, “Gr.T.Popa” University of Medicine and Pharmacy, No. 16 Universitatii Street, 700115, Iasi, Romania
  • Department of Histology, School of Medicine, “Gr.T.Popa” University of Medicine and Pharmacy, No. 16 Universitatii Street, 700115, Iasi, Romania
  • Clinical Hospital Diseases “Sf. Parascheva”, No. 2 Octav Botez Street, 700116, Iasi, Romania
  • [1] Dorschei D.R, Wojcik K.R., Sun S., Marroquin B., White S.R., Apoptosis of airway epithelial cells induced by corticosteroids, Am. J. Respir. Crit. Care Med., 2001, 164:1939–47
  • [2] Zalewki P.D., Ruffin R.E., Apoptosis-regulatory factors as potential drug targets in the epithelium of normal and inflamed airways, Curr. Mol. Pharmacol., 2008, 1:38–49[Crossref]
  • [3] Vignola A.M., Chiappara G., Siena L., Bruno A., Gagliardo R., Merendino A.M., et al., Proliferation and activation of bronchial epithelial cells in corticosteroid-dependent asthma, J. Allergy Clin. Immunol., 2001, 108(5):738–46[Crossref]
  • [4] Druilhe A., Wallaert B., Tsicopoulos A., Lapa e Silva J-R., Tillie-Lillie-Leblond I., Tonnel A.B., et al., Apoptosis, Proliferation, and Expression of Bcl-2, Fas, and Fas Ligand in Bronchial Biopsies from Asthmatics, Am. J. Respir. Cell. Mol. Biol., 1998, 19(5):747–757 [Crossref]
  • [5] Vignola A.M., Mirabella F., Constanzo G., Mark Gjomarkaj R., Bellia V., Bonsignore G., Airway remodeling in asthma, Chest, 2003, 123:417S–4422S[Crossref]
  • [6] Cohen L., Tarsi J., Ramkumar T., Horiuchi T.K., Cochran R., DeMartino S., et al., and the NHLBI Severe Asthma Research Program (SSARP), Epithelial cell proliferation contributes to airway remodeling in severe asthma, Am. J. Respir. Crit. Care Med., 2007, 15;176(2):138–45. Epub 2007 Apr 26[Crossref]
  • [7] Sidhu G.S., Singh A.K., Banaudha K.K., Arnebin-1 accelerates normal and hydrocortisone-induced impaired wound healing, J. Invest. Dermatol., 1999, 113:7773–781[Crossref]
  • [8] Feng Z., Marti A., Jehn B., Glucocorticoid and progesterone inhibit involution and programmed cell death in the mouse mammary gland, J. Cell. Biol., 1995, 131:1095–1103[Crossref]
  • [9] Harris R.A., Hiles I.D., Page M.J., The induction of apoptosis in human mammary luminal epithelial cells by expression of activated c-neu and its abrogation by glucocorticoids, Br. J. Cancer 1995, 72:386–392
  • [10] Wen L.-PP, Madani K., Fahrni J.A., Duncan S.R., Rosen G.D., Dexamethasone inhibits lung epithelial cell apoptosis induced by IFN- and Fas, Am. J. Physiol., 1997, 273:L921–L929
  • [11] Dorscheid D.R., Wojcik K.R., Sun S., Marroquin B., White S. R., Apoptosis of Airway Epithelial Cells Induced by Corticosteroids, Am. J. Respir. Crit. Care Med., 2001, 164(10):1939–1947
  • [12] White S.R., Dorscheid D.R., Corticosteroid-Induced Apoptosis of Airway Epithelium - A Potential Mechanism for Chronic Airway Epithelial Damage in Asthma, Chest, 2002, 22:2278S–2284S
  • [13] Rogers D.F., The airway goblet cell, Int. J. Biochem. Cell Biol., 2003, 35(1):1–6[Crossref]
  • [14] Rogers D.F., Airway goblet cells: responsive and adaptable front-line defenders, Eur Respir. J., 1994, 7(9):1690–706[Crossref]
  • [15] Fahy J.V., Goblet cell and mucin gene abnormalities in sthma, Chest, 2002, 22(66 Suppl):3320S–3326S
  • [16] Rogers D.F., Barnes P.JJ., Treatment of airway mucus hypersecretion, Ann. Med., 2006, 38(2):116–25[Crossref]
  • [17] Schwalm K., Stevens J.F., Jiang Z., Expression of the proapoptotic protein Bax is reduced in bronchial mucous cells of asthmatic subjects, Am. J. Physiol. Lung Cell. Mol. Physiol., 2008, 294(6):L1102–9[WoS][Crossref]
  • [18] Shi Z.Q., Feng Y., Hou Y.KK., Liu T., Xiu Q.Y., A study of interferon-gamma induced airway mucous cell apoptosis and its mechanisms, Zhonghua Jie He He Hu Xi Za Zhi, 2005, 28(3):160–3
  • [19] Xiang J., Rir-Sim-Ah J., Tesfaigzi Y., IL-9 and IL-13 induce mucous cell metaplasia that is reduced by IFN-gamma in a Bax-mediated pathway, Am. J.Respir. Cell. Mol. Biol., 2008, 38(33):3310–7. Epub 2007 ep 7 [WoS]
  • [20] Lindsten T., Ross A.J., King A., The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues, Mol. Cell., 2000, 6:1389–99[Crossref]
  • [21] Nechushtan A., Smith C.L., Lamensdorf I., Bax and Bak coalesce into novel mitochondria-aassociated clusters during apoptosis, J. Cell. Biol., 2001;153:1265–76[Crossref]
  • [22] Tsujimoto Y., Shimizu S., VDAC regulation by the Bcl-2 family of proteins, Cell. Death. Differ., 2000, 7:1174–81[Crossref][WoS]
  • [23] Denault J.B., Salvesen G.S., Caspases: keys in the ignition of cell death, Chem. Rev., 2002, 102:4489–99[Crossref]
  • [24] Kromer G., Galluzzi L., Brenner C., Mitochondrial membrane permeabilization in cell deth, Physiol. Rev., 2007, 87:99–163[Crossref]
  • [25] Kromer G., Reed J.C., Mitochondrial control of cell death, Nat. Med., 2000, 6:513–19[Crossref]
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