EXPERIMENTAL
CELL
RESEARCH
195,
214-217
(1991)
Regulation by Epidermal Growth Factor of the Expression of Transforming Growth Factor-@1 mRNA in Cultured Rat Liver Epithelial Cells MING-SOUND *Lkpartmcnt tlkpartment
o/ Pathology, of Pathology,
TSAO,*B’ XIAO-YAN
ZHANG,*
Montreal Gmwal Hospital and McGill C’niuersity of North Carolina School
Expression of transforming growth factor (TGF)-/31 mRNA in cultured rat liver epithelial cells is stimulated by epidermal growth factor (EGF), and this increased expression reflects enhanced transcription of the gene. Transient stimulation of TGF-P expression by EGFi TGF-(Y may function as the mechanism for control of stimulated cell proliferation, such as that typified by liver regeneration. c 1991 Academic I’ress, Inc.
INTRODUCTION Transforming growth factor-$ (TGF-0) belongs to a large family of multifunctional polypeptides which have important and diverse biological and biochemical effects on cells. These peptides regulate cellular proliferation, differentiation, and function during normal embryogenesis and development and during pathological processes such as inflammation and repair, regeneration, and neoplasia [l-4]. Several molecular forms of TGF-/3 have been recognized, at least three of which (81, 02, and /33) share 70-80s homology in amino acid sequences [2]. These TGF-P isoforms are functionally cross-reactive with their respective receptors but show differential potency in their effects depending on cell type and assay used, and they are also differentially expressed in various cells and tissues. TGF-/3s are found at highest concentrations in platelets and bone, but they are expressed ubiquitously, albeit at varying levels, in almost all organs and tissues examined, as well as in cultured cells [1,2,8,9]. During embryogenesis, expression of both TGF-01 and -02 shows unique spatial and temporal patterns which are highly associated with the formation of mesodermal and mesenchymal tissues, especially in tissues in which critical mesenchymal-epithelial interactions occur [ 10-141. Although extensive stud-
’ To whom all correspondence and reprint requests should he addressed at: Department of Pathology, Montreal General Hospital, 1650 Cedar Avenue, Montreal, Quebec, H3G 1A4, Canada.
0014.4827/91 Copyright All rights
$3.00 c 1991 by Academic Press, of reproduction in any form
214 Inc. reserved.
CHI LIU,* ( ‘niuersity,
of Medicine,
AND
JOE W. GRISHAM?
Montreal, Quebec, Canada, Chap. Biochem. Biophys. Km. C’ommun. 157, 1049-1045. 29. Merlino, G. T., Xu, Y.-H., Ishii, S., Clark, A. J. L., Semba, K., Toyoshima,
REFERENCES
K., Yamamoto,
T., and Pastan,
I. .Scicnce (Washing
ton D.C.) 224, 417-419.
Roberts, A. B., Flanders, K. C., Konaiah, P., Thompson, N. I,., Van Obberghen-Schilling, E., Wakefield, L., Rossi, P., de Crombrugghe, B., Heine. V., and Spom, M. B. (1988) Rec. Pro,q. Horn. Rrs. 44, 157-197.
30. Derynck,
2.
Roberts, A. B., Thompson. N. L., Heine, V., Flanders, Sporn, M. R. (1988) Br. J. Cancrr 57, 594-600.
:3.
Sporn, M. B., Roberts, A. B., Wakefield, L. M., and de Crombrugghe, B. (1987) J. Cell Riol. 105, 1039%1045. Massague, J. I 1987) Cell 49, 437-438. Cheifetz, S., Weatherbee, J. A., Tsang, M. L.-S.,Anderson, J. K., Mole, J. E., Lucas, R., and Massague, J. (1987) Cell 48,409-415. ten Dijke, P., Hanser, P., Iwata, K. K., Pieler, C., and Foulkes, J. G. (1988) Proc. Nat/. Acad. Sci. USA 85, 4715-4719. Graycar, J. L., Miller, D. A., Arrick, B. A., Lyons, R. M., Moses, H. L., and Derynck, R. (1989) Mol. E’ndocrinol. 3, 1977-1986. Derynck, R., Goeddel, D. V., Ullrich, A., Gutterman, J. V., Williams, R. D., Bringman, T. S., and Berger, W. H. (1987) Cancer Rcs. 47, 707-71’. Miller, I). A., Lee, A., Pelton, R. W., Chen, E. Y., Moses, H. L., and Derynck, R. (1989) Mol. Endocrinol. 3, 1108-1114.
32. Lin, P., Liu, C., Tsao, M.-S., and Grisham, .J. W. (1987) Biochem. Biophys. Rcs. C’ommun. 143, 26-30. 33. Kim, S.-J., cJeang, K. T., Glick, A. B., Sporn, M. B., and Roberts,
1.
4. 5. 6. 7. 8.
9.
Received Revised
December 27, 1990 version received March
11. 1991
C., and
Bid 31.
P., Jarrett,
(‘hem.
Tsao,
M.-S.,
,J. A., Chen,
E. Y., and Goeddel,
D. V. J.
261, 4377-4379. Earp,
H. S.. and Grisham,
J. W. (1986)
J. Ceil. Ph,vs-
id. 126, 167-193.
34. 35.
A. B. (1989) J. Biol. (‘hem. 264, 7041-7045. Grisham, J. W. (1962) Cancer Res. 22,842~849. Rabes, H. M., Wirsching, Tissue Kinet. 9, 51 i-532.
R., Tuczek,
H.-V.,
and Iseler,
G. Cell
36. Mead, J. E., and Fausto, E. (1989) Proc. dVutl. Acad. Sci. lJ.SA 86,1558-1562. 37. Braun, L., Mead, J. E., Panzica, M., Mikumo, R., Bell, G. I., and Fausto,
38. Russell, (1988)
N. (1988)
Proc. Natl.
Acad.
Sci. USA
85,
1539-1543.
W. E., Coffey Jr, R. J., Ouellette, A. J., and Moses, Proc. Natl. Acad. Sci. 1JSA 85, 5126-5130.
39. Fausto, N., and Mead, J. E. (1989) Lab. Incest.60, 4-13. 40. Michalopoulos, G. K. (1990) FASEB J. 4, 176-187.
H. L.
CELL
RESEARCH
195,
214-217
(1991)
Regulation by Epidermal Growth Factor of the Expression of Transforming Growth Factor-@1 mRNA in Cultured Rat Liver Epithelial Cells MING-SOUND *Lkpartmcnt tlkpartment
o/ Pathology, of Pathology,
TSAO,*B’ XIAO-YAN
ZHANG,*
Montreal Gmwal Hospital and McGill C’niuersity of North Carolina School
Expression of transforming growth factor (TGF)-/31 mRNA in cultured rat liver epithelial cells is stimulated by epidermal growth factor (EGF), and this increased expression reflects enhanced transcription of the gene. Transient stimulation of TGF-P expression by EGFi TGF-(Y may function as the mechanism for control of stimulated cell proliferation, such as that typified by liver regeneration. c 1991 Academic I’ress, Inc.
INTRODUCTION Transforming growth factor-$ (TGF-0) belongs to a large family of multifunctional polypeptides which have important and diverse biological and biochemical effects on cells. These peptides regulate cellular proliferation, differentiation, and function during normal embryogenesis and development and during pathological processes such as inflammation and repair, regeneration, and neoplasia [l-4]. Several molecular forms of TGF-/3 have been recognized, at least three of which (81, 02, and /33) share 70-80s homology in amino acid sequences [2]. These TGF-P isoforms are functionally cross-reactive with their respective receptors but show differential potency in their effects depending on cell type and assay used, and they are also differentially expressed in various cells and tissues. TGF-/3s are found at highest concentrations in platelets and bone, but they are expressed ubiquitously, albeit at varying levels, in almost all organs and tissues examined, as well as in cultured cells [1,2,8,9]. During embryogenesis, expression of both TGF-01 and -02 shows unique spatial and temporal patterns which are highly associated with the formation of mesodermal and mesenchymal tissues, especially in tissues in which critical mesenchymal-epithelial interactions occur [ 10-141. Although extensive stud-
’ To whom all correspondence and reprint requests should he addressed at: Department of Pathology, Montreal General Hospital, 1650 Cedar Avenue, Montreal, Quebec, H3G 1A4, Canada.
0014.4827/91 Copyright All rights
$3.00 c 1991 by Academic Press, of reproduction in any form
214 Inc. reserved.
CHI LIU,* ( ‘niuersity,
of Medicine,
AND
JOE W. GRISHAM?
Montreal, Quebec, Canada, Chap. Biochem. Biophys. Km. C’ommun. 157, 1049-1045. 29. Merlino, G. T., Xu, Y.-H., Ishii, S., Clark, A. J. L., Semba, K., Toyoshima,
REFERENCES
K., Yamamoto,
T., and Pastan,
I. .Scicnce (Washing
ton D.C.) 224, 417-419.
Roberts, A. B., Flanders, K. C., Konaiah, P., Thompson, N. I,., Van Obberghen-Schilling, E., Wakefield, L., Rossi, P., de Crombrugghe, B., Heine. V., and Spom, M. B. (1988) Rec. Pro,q. Horn. Rrs. 44, 157-197.
30. Derynck,
2.
Roberts, A. B., Thompson. N. L., Heine, V., Flanders, Sporn, M. R. (1988) Br. J. Cancrr 57, 594-600.
:3.
Sporn, M. B., Roberts, A. B., Wakefield, L. M., and de Crombrugghe, B. (1987) J. Cell Riol. 105, 1039%1045. Massague, J. I 1987) Cell 49, 437-438. Cheifetz, S., Weatherbee, J. A., Tsang, M. L.-S.,Anderson, J. K., Mole, J. E., Lucas, R., and Massague, J. (1987) Cell 48,409-415. ten Dijke, P., Hanser, P., Iwata, K. K., Pieler, C., and Foulkes, J. G. (1988) Proc. Nat/. Acad. Sci. USA 85, 4715-4719. Graycar, J. L., Miller, D. A., Arrick, B. A., Lyons, R. M., Moses, H. L., and Derynck, R. (1989) Mol. E’ndocrinol. 3, 1977-1986. Derynck, R., Goeddel, D. V., Ullrich, A., Gutterman, J. V., Williams, R. D., Bringman, T. S., and Berger, W. H. (1987) Cancer Rcs. 47, 707-71’. Miller, I). A., Lee, A., Pelton, R. W., Chen, E. Y., Moses, H. L., and Derynck, R. (1989) Mol. Endocrinol. 3, 1108-1114.
32. Lin, P., Liu, C., Tsao, M.-S., and Grisham, .J. W. (1987) Biochem. Biophys. Rcs. C’ommun. 143, 26-30. 33. Kim, S.-J., cJeang, K. T., Glick, A. B., Sporn, M. B., and Roberts,
1.
4. 5. 6. 7. 8.
9.
Received Revised
December 27, 1990 version received March
11. 1991
C., and
Bid 31.
P., Jarrett,
(‘hem.
Tsao,
M.-S.,
,J. A., Chen,
E. Y., and Goeddel,
D. V. J.
261, 4377-4379. Earp,
H. S.. and Grisham,
J. W. (1986)
J. Ceil. Ph,vs-
id. 126, 167-193.
34. 35.
A. B. (1989) J. Biol. (‘hem. 264, 7041-7045. Grisham, J. W. (1962) Cancer Res. 22,842~849. Rabes, H. M., Wirsching, Tissue Kinet. 9, 51 i-532.
R., Tuczek,
H.-V.,
and Iseler,
G. Cell
36. Mead, J. E., and Fausto, E. (1989) Proc. dVutl. Acad. Sci. lJ.SA 86,1558-1562. 37. Braun, L., Mead, J. E., Panzica, M., Mikumo, R., Bell, G. I., and Fausto,
38. Russell, (1988)
N. (1988)
Proc. Natl.
Acad.
Sci. USA
85,
1539-1543.
W. E., Coffey Jr, R. J., Ouellette, A. J., and Moses, Proc. Natl. Acad. Sci. 1JSA 85, 5126-5130.
39. Fausto, N., and Mead, J. E. (1989) Lab. Incest.60, 4-13. 40. Michalopoulos, G. K. (1990) FASEB J. 4, 176-187.
H. L.
