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Typus
Verschleierung
Bearbeiter
PlagProf:-)
Gesichtet
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Untersuchte Arbeit:
Seite: 14, Zeilen: 1-30
Quelle: Fehrenbach_2001
Seite(n): 40, 41, Zeilen: S. 40: letzter Absatz, S. 41: 1ff
[Additionally, AECII9] have direct contact to fibroblasts at the basal membrane or with capillary endothelial cells (Marin et al., 1982).

A strong evidence for a direct interaction of AECI and AECII was presented by Ashino and colleagues (Ashino et al., 2000). Mechanical stimulation of AECI is thought to result in Ca2+-oscillations, which were transmitted via intraepithelial gap junctions to AECII and modulate exocytosis rate of lamellar bodies. Direct inhibitory interactions between AECI and AECII have been postulated to suppress AECII proliferation. Loss of AECI during injury might then trigger the release of AECII from growth inhibition (Mason and McCormack, 1994). E-cadherin as a further candidate to mediate contact inhibition, has been localized to the basolateral membrane of AECII (Kasper et al., 1995; St. Croix et al., 1998).

But even an indirect cell-cell interaction for AECII to other AECII is possible by the negative feedback loop by which surfactant protein A (SP-A) upon release into the alveolar space inhibits surfactant exocytosis in vitro (Dobbs et al., 1987). Although AECII are equipped with membrane receptors for SP-A (Strayer et al., 1996), the in vivo relevance of this autocrine mechanism by which AECII may regulate their own action remains elusive, because mice that are deficient in SP-A did not show any defect in surfactant secretion nor any respiratory deficiency (Ikegami et al., 1998). Thus, some alternative mechanism must compensate the negative SP-A feedback loop. Another potential feedback mechanism that has been postulated is the inhibition of AECII proliferation via AECII derived transforming growth factor (TGF)-β in bleomycin-induced experimental lung fibrosis (Khali et al., 1994). A number of growth factors are released by AECII, which might act in an autocrine way via the corresponding receptors expressed by AECII.

As mentioned before, fibroblasts are in contact to AECII. This reciprocal cell-cell interaction is relevant to the modelling of alveolus during lung morphogenesis as well as during remodelling associated with alveolar repair following lung injury (Kasper et al., 1996; O´Reilly et al., 1997; Shannon, et al., 1997). Both direct and indirect cell-cell interactions have been reported.


Dobbs LG, Wright JR, Hawgood S, Gonzalez R, Venstrom K, Nellenbogen J. Pulmonary surfactant and its components inhibit secretion of phosphatidylcholine from cultured rat alveolar type II cells. Proc Natl Acad Sci U S A. 1987 Feb; 84 (4): 1010-4.

Ikegami M, Korfhagen TR, Whitsett JA, Bruno MD, Wert SE, Wada K, Jobe AH. Characteristics of surfactant from SP-A-deficient mice. Am J Physiol. 1998 Aug; 275 (2Pt1): L247-54.

Kasper M, Traub O, Reimann T, Bjermer L, Grossmann H, Muller M, Wenzel KW Upregulation of gap junction protein connexin43 in alveolar epithelial cells of rats with radiation-induced pulmonary fibrosis. Histochem Cell Biol. 1996 Oct; 106 (4): 419-24.

Kasper M, Huber O, Grossmann H, Rudolph B, Trankner C, Muller M. Immunocytochemical distribution of E-cadherin in normal and injured lung tissue of the rat. Histochem Cell Biol. 1995 Nov; 104 (5): 383-90.

Khalil N, O'Connor RN, Flanders KC, Shing W, Whitman CI. Regulation of type II alveolar epithelial cell proliferation by TGF-beta during bleomycin-induced lung injury in rats. Am J Physiol. 1994 Nov; 267 (5Pt1): L498-507.

Marin L, Dameron F, Relier JP. Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate. 1982; 41 (3-4): 172-82.

Mason RJ, McCormack FX. Alveolar type II cell reactions in pathogenic states. In Lung surfactant:Basic research in the pathogenesis of lung disorders. Edited by Müller B, von WichertP. Basel; Karger, 1994: 194-204.

O'Reilly MA, Stripp BR, Pryhuber GS. Epithelial-mesenchymal interactions in the alteration of gene expression and morphology following lung injury. Microsc Res Tech. 1997 Sep 1; 38 (5): 473-9. Review.

Shannon JM, Deterding RR Epithelial-mesenchymal interactions in lung development. In Lung growth and development. Edited by Mc Donald JA. New York; Marcel Dekker, Inc., 1997: 81-118.

St Croix B, Sheehan C, Rak JW, Florenes VA, Slingerland JM, Kerbel RS. E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1). J Cell Biol. 1998 Jul 27; 142 (2): 557-71.

Strayer DS, Pinder R, Chander A. Receptor-mediated regulation of pulmonary surfactant secretion. Exp Cell Res. 1996 Jul 10; 226 (1): 90-7.

The basal cell membrane is in close proximity to fibroblasts, in particular during the canalicular phase of lung morphogenesis, while modelling of the alveolar septum results in an increase in the spatial relationship of the AE2 cells with capillary endothelial cells of the adult lung [143].

The in situ study of Ashino and co-workers [64] presented strong evidence of a direct interaction of AE1 and AE2 cells. Mechanical stimulation of AE1 cells is thought to result in [Ca2+]i-oscillations (see above), which are transmitted via interepithelial gap junctions to AE2 cells and modulate exocytosis rate of lamellar bodies [64]. Direct inhibitory interactions between AE1 and AE2 cells have been postulated to suppress AE2 cell proliferation [144].

Loss of AE1 cells during lung injury might then be the trigger to release AE2 cells from growth inhibition. Although E-cadherin, a candidate mediator of contact inhibition [145], has been localised to the basolateral membrane of adult human AE2 cells [146], experimental evidence for contact inhibition of AE2 cell proliferation by AE1 cells still remains to be presented.

The most intensely studied example of an indirect AE2–AE2 cell interaction is probably the negative feedback loop by which SP-A, released into the alveolar space, inhibits surfactant exocytosis in vitro [69]. Although AE2 cells are equipped with membrane receptors for SPA [70], the in vivo relevance of this autocrine mechanism by which AE2 cells may regulate their own action is still not convincing (as pointed out recently [52]). Since mice that are deficient for SP-A did not show any defect in surfactant secretion nor any respiratory deficiency [147], there must be some alternative mechanism compensating for the loss of a SP-A feedback loop, if present at all.

Another potential feedback mechanism that has been postulated is the inhibition of AE2 cell proliferation via AE2-cell-derived transforming growth factor (TGF)-b in bleomycin-induced experimental lung fibrosis [148]. A number of growth factors are released by AE2 cells, which might act in an autocrine way via the corresponding receptors expressed by AE2 cells (see Supplementary Table 2).

Fibroblasts

The interaction of AE2 cells with fibroblasts is probably the best studied reciprocal cell-cell relationship which is relevant to the modelling of alveoles during lung morphogenesis (for review see, eg, [149]) as well as during remodelling associated with alveolar repair following lung injury (for review see, eg, [123,150]). Both direct and indirect cell-cell interactions have been reported, in most instances from studies of cells grown in culture.


143. Marin L, Dameron F, Relier JP: Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate 1982, 41:172–182.

64. Ashino Y, Ying X, Dobbs LG, Bhattacharya J: [Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus. Am J Physiol Lung Cell Mol Physiol 2000, 279:L5–13.

144. Mason RJ, McCormack FX: Alveolar type II cell reactions in pathologic states. In Lung surfactant: Basic research in the pathogenesis of lung disorders. Edited by Müller B, von Wichert P. Basel; Karger, 1994:194–204.

145. St. Croix B, Sheehan C, Rak JW, Florenes VA, Slingerland JM, Kerbel RS: E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1). J Cell Biol 1998, 142:557–571.

146. Kasper M, Behrens J, Schuh D, Müller M: Distribution of E-cadherin and Ep-CAM in the human lung during development and after injury. Histochem Cell Biol 1995, 103:281–286.

69. Dobbs LG, Wright JR, Hawgood S, Gonzalez R, Venstrom K, Nellenbogen J: Pulmonary surfactant and its components inhibit secretion of phosphatidylcholine from cultured rat alveolar type II cells. Proc Natl Acad Sci U S A 1987, 84:1010–1014.

70. Strayer DS, Pinder R, Chander A: Receptor-mediated regulation of pulmonary surfactant secretion. Exp Cell Res 1996, 226:90–97.

52. Rooney SA: Regulation of surfactant secretion. In Lung surfactant: cellular and molecular processing. Edited by Rooney SA. Austin, Texas; RG Landes Company, 1998:139–163.

123. Kasper M, Haroske G: Alterations in the alveolar epithelium after injury leading to pulmonary fibrosis. Histol Histopathol 1996, 11:463–483.

150. O’Reilly MA, Stripp BR, Pryhuber GS: Epithelial-mesenchymal interactions in the alteration of gene expression and morphology following lung injury. Microsc Res Tech 1997, 38:473–479.

147. Ikegami M, Korfhagen TR, Whitsett JA, Bruno MD, Wert SE, Wada K, Jobe AH: Characteristics of surfactant from SP-Adeficient mice. Am J Physiol 1998, 275:L247–254.

148. Khalil N, O’Connor RN, Flanders KC, Shing W, Whitman CI: Regulation of type II alveolar epithelial cell proliferation by TGFbeta during bleomycin-induced lung injury in rats. Am J Physiol 1994, 267:L498–507.

149. Shannon JM, Deterding RR: Epithelial-mesenchymal interactions in lung development. In Lung growth and development. Edited by McDonald JA. New York; Marcel Dekker, Inc., 1997: 81–118.

Anmerkungen

In pp. 13-16, the author adopts an uninterrupted review of some 30 articles from Fehrenbach without indicating this source.

Sichter
Hindemith

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