The Experts below are selected from a list of 21 Experts worldwide ranked by ideXlab platform

Friedrich Thaiss - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin e1 inhibits collagen expression in anti Thymocyte Antibody induced glomerulonephritis possible role of tgfβ
    Kidney International, 1996
    Co-Authors: Andre Schneide, Friedrich Thaiss, Hanspete Rau, Gunte Wolf, Gunthe Zahne, Thomas Jocks
    Abstract:

    Prostaglandin E1 inhibits collagen expression in anti-Thymocyte Antibody-induced glomerulonephritis: Possible role of TGFβ. To test whether or not prostaglandins mediate extracellular matrix formation in immune-mediated glomerular disease, rats with anti-Thymocyte Antibody-induced glomerulonephritis were treated with prostaglandin E1 (PGE 1 ) (250 μ g/twice daily/s.c.). Glomerular expression of collagen types III and IV was assessed by Northern blotting, immunohistology and Western blotting. Proliferation of glomerular cells was evaluated by staining for the proliferating cell nuclear antigen (PCNA) and consecutive cell counting. At day five after induction of the disease, glomerular mRNA levels of collagen types III and IV were three- to fivefold higher compared with non-nephritic controls. Similarly glomerular deposition of these collagens was markedly increased when assessed by immunohistology. The treatment of nephritic rats with PGE 1 reduced the increased glomerular mRNA levels as well as the protein concentration and the deposition of extracellular collagens. The number of PCNA positive cells which was significantly higher in nephritic rats when compared with control animals (24 hr, nephritis 2.53 ± 0.33 and Control 0.26 ± 0.06, P = 0.011; 5 days, nephritis 5.10 ± 1.13 and Control 0.75 ± 0.08, cells per glomerular cross section, P = 0.03) was reduced by PGE 1 (24 hr, nephritis + PGE 1 0.44 ± 0.30, P=0.0001; 5 days, nephritis + PGE 1 1.91 ± 1.84 cells per glomerular cross section, P = 0.001). Prostaglandin E 1 also ameliorated the glomerular infiltration of monocytes at 24 hours (nephritis 4.36 ± 2.82, nephritis + PGE 1 2.20 ± 1.82, cells per glomerular cross section) and five days (nephritis 1.51 ± 0.58, nephritis + PGE 1 1.12 ± 0.61, cells per glomerular cross section). To further characterize possible mechanisms by which PGE 1 reduces extracellular matrix deposition, the glomerular expression of transforming growth factor (TGF- β ), and interleukin 1 β (IL-1 β ) was assessed by Northern blotting. Nephritic glomeruli showed increased mRNA levels of TGF- β at day 5 and IL-1 β at 24 hours when compared with control kidneys. Treatment of the animals with PGE 1 inhibited the mRNA expression of TGF- β and IL-1 β . These data demonstrate that PGE 1 reduces the glomerular expression of extracellular matrix proteins in anti-Thymocyte Antibody-induced glomerulonephritis, suggesting a beneficial role of prostaglandins in this proliferative glomerular immune injury. The effects of PGE 1 might be mediated by inhibition of TGF- β and IL-1 β production.

  • prostaglandin e1 reduces the glomerular mrna expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerular injury
    Journal of The American Society of Nephrology, 1996
    Co-Authors: Thomas Jocks, Friedrich Thaiss, Gunte Wolf, Gunthe Zahne, J Freudenberg, Udo Helmche, R A K Stahl
    Abstract:

    To study whether prostaglandins (PG) can regulate the mRNA expression of monocyte-chemoattractant protein 1 (MCP-1) in glomerular immune injury, MCP-1 mRNA levels were evaluated in anti-Thymocyte Antibody (ATS) -induced glomerular injury by Northern blotting and reverse transcription-polymerase chain reaction. Immune injury was induced in vivo by the intravenous application of ATS to male Wistar rats and in vitro by the perfusion of isolated rat kidneys with ATS and rat serum. In vivo 3 h and 5 days after Antibody application, glomerular mRNA expression of MCP-1 was markedly enhanced compared with controls. In the isolated perfused kidney, Antibody and complement also induced an increase in MCP-1 expression at 10 min and 60 min after Antibody perfusion. When the rats were treated with PGE (250 micrograms, twice daily), the increase in MCP-1 expression was reduced. This was associated with a reduction of intraglomerular recruitment of monocytes/macrophages. In the isolated perfused kidneys, PGE1 (1 mg/L) prevented the Antibody- and rat serum-stimulated increase in glomerular MCP-1 mRNA expression. These data demonstrate that PGE1 reduces glomerular MCP-1 mRNA expression in glomerulonephritis and in the isolated perfused rat kidney after induction of immune injury with Antibody and complement. The data suggest that prostaglandins might mediate MCP-1 effects in glomerular immune injuries.

  • increased expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerulonephritis
    Kidney International, 1993
    Co-Authors: Friedrich Thaiss, R A K Stahl, Martina Disse, Udo Helmche
    Abstract:

    Increased expression of monocyte chemoattractant protein-1 in anti-Thymocyte Antibody-induced glomerulonephritis. The infiltration of monocytes-macrophages in the glomerulus is one of the hallmarks of glomerulonephritis and may play an important pathogenetic role. Monocyte chemoattractant protein-1 (MCP-1) and colony stimulating factor-1 (CSF-1) are monocyte-specific cytokines with chemoattractant and activating activities for monocytes. MCP-1 and CSF-1 can be generated by several cell types, including glomerular mesangial cells, and can be stimulated by cytokines and immune complexes. To study the expression of CSF-1 and MCP-1 in a model of proliferative glomerulonephritis we used Northern blot analysis and immuno-histochemistry. The glomerular lesion was induced in rats by the i.v. injection of a heterologous anti-Thymocyte antiserum (ATS), directed against an antigen which is localized on glomerular mesangial cells. Northern blot analysis revealed comparable amounts of CSF-1 in glomeruli isolated from control untreated rats, and from rats after 30 minutes to three weeks of injection of ATS Antibody. In control glomeruli no mRNA levels for MCP-1 were detectable, but increased markedly 30 minutes after the induction of the nephritis, were then reduced at 24 hours and increased again at 5 and 21 days after induction of the disease. The increase in mRNA levels for MCP-1 30 minutes or 24 hours after ATS injection was markedly attenuated if rats were complement depleted by cobra venom injection. These time points following Antibody injection were associated with mesangial immune complex formation (30 min), mesangiolysis (24 hr) and proliferative glomerulonephritis (5 and 21 days). By immunohistology the presence of MCP-1 was demonstrated in glomeruli with a predominant mesangial distribution. The mesangial immunofluorescence for MCP-1 followed a pattern similar to that of the mRNA for MCP-1 after induction of the disease process, that is, it increased after 30 minutes, decreased after 24 hours and was increased again at three weeks. Within 30 minutes of the Antibody injection an increased infiltration of monocytes-macrophages was observed in the glomeruli, which was maintained up to three weeks of induction of the glomerulonephritis. When the rats were decomple-mented with cobra venom factor prior to the i.v. injection of ATS, the expression of MCP-1 in glomeruli remained low and the influx of monocytes/macrophages did not appear. We conclude that MCP-1 is increased early on in glomeruli of rats with immune-mediated mesangial proliferative glomerulonephritis. This increase is mediated by complement activation secondary to the in situ immune complex formation at the glomerular mesangium. Elevated MCP-1 might play an important role in the recruitment of monocytes/macrophages into glomeruli following in situ immune complex formation.

R A K Stahl - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin e1 reduces the glomerular mrna expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerular injury
    Journal of The American Society of Nephrology, 1996
    Co-Authors: Thomas Jocks, Friedrich Thaiss, Gunte Wolf, Gunthe Zahne, J Freudenberg, Udo Helmche, R A K Stahl
    Abstract:

    To study whether prostaglandins (PG) can regulate the mRNA expression of monocyte-chemoattractant protein 1 (MCP-1) in glomerular immune injury, MCP-1 mRNA levels were evaluated in anti-Thymocyte Antibody (ATS) -induced glomerular injury by Northern blotting and reverse transcription-polymerase chain reaction. Immune injury was induced in vivo by the intravenous application of ATS to male Wistar rats and in vitro by the perfusion of isolated rat kidneys with ATS and rat serum. In vivo 3 h and 5 days after Antibody application, glomerular mRNA expression of MCP-1 was markedly enhanced compared with controls. In the isolated perfused kidney, Antibody and complement also induced an increase in MCP-1 expression at 10 min and 60 min after Antibody perfusion. When the rats were treated with PGE (250 micrograms, twice daily), the increase in MCP-1 expression was reduced. This was associated with a reduction of intraglomerular recruitment of monocytes/macrophages. In the isolated perfused kidneys, PGE1 (1 mg/L) prevented the Antibody- and rat serum-stimulated increase in glomerular MCP-1 mRNA expression. These data demonstrate that PGE1 reduces glomerular MCP-1 mRNA expression in glomerulonephritis and in the isolated perfused rat kidney after induction of immune injury with Antibody and complement. The data suggest that prostaglandins might mediate MCP-1 effects in glomerular immune injuries.

  • increased expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerulonephritis
    Kidney International, 1993
    Co-Authors: Friedrich Thaiss, R A K Stahl, Martina Disse, Udo Helmche
    Abstract:

    Increased expression of monocyte chemoattractant protein-1 in anti-Thymocyte Antibody-induced glomerulonephritis. The infiltration of monocytes-macrophages in the glomerulus is one of the hallmarks of glomerulonephritis and may play an important pathogenetic role. Monocyte chemoattractant protein-1 (MCP-1) and colony stimulating factor-1 (CSF-1) are monocyte-specific cytokines with chemoattractant and activating activities for monocytes. MCP-1 and CSF-1 can be generated by several cell types, including glomerular mesangial cells, and can be stimulated by cytokines and immune complexes. To study the expression of CSF-1 and MCP-1 in a model of proliferative glomerulonephritis we used Northern blot analysis and immuno-histochemistry. The glomerular lesion was induced in rats by the i.v. injection of a heterologous anti-Thymocyte antiserum (ATS), directed against an antigen which is localized on glomerular mesangial cells. Northern blot analysis revealed comparable amounts of CSF-1 in glomeruli isolated from control untreated rats, and from rats after 30 minutes to three weeks of injection of ATS Antibody. In control glomeruli no mRNA levels for MCP-1 were detectable, but increased markedly 30 minutes after the induction of the nephritis, were then reduced at 24 hours and increased again at 5 and 21 days after induction of the disease. The increase in mRNA levels for MCP-1 30 minutes or 24 hours after ATS injection was markedly attenuated if rats were complement depleted by cobra venom injection. These time points following Antibody injection were associated with mesangial immune complex formation (30 min), mesangiolysis (24 hr) and proliferative glomerulonephritis (5 and 21 days). By immunohistology the presence of MCP-1 was demonstrated in glomeruli with a predominant mesangial distribution. The mesangial immunofluorescence for MCP-1 followed a pattern similar to that of the mRNA for MCP-1 after induction of the disease process, that is, it increased after 30 minutes, decreased after 24 hours and was increased again at three weeks. Within 30 minutes of the Antibody injection an increased infiltration of monocytes-macrophages was observed in the glomeruli, which was maintained up to three weeks of induction of the glomerulonephritis. When the rats were decomple-mented with cobra venom factor prior to the i.v. injection of ATS, the expression of MCP-1 in glomeruli remained low and the influx of monocytes/macrophages did not appear. We conclude that MCP-1 is increased early on in glomeruli of rats with immune-mediated mesangial proliferative glomerulonephritis. This increase is mediated by complement activation secondary to the in situ immune complex formation at the glomerular mesangium. Elevated MCP-1 might play an important role in the recruitment of monocytes/macrophages into glomeruli following in situ immune complex formation.

Thomas Jocks - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin e1 inhibits collagen expression in anti Thymocyte Antibody induced glomerulonephritis possible role of tgfβ
    Kidney International, 1996
    Co-Authors: Andre Schneide, Friedrich Thaiss, Hanspete Rau, Gunte Wolf, Gunthe Zahne, Thomas Jocks
    Abstract:

    Prostaglandin E1 inhibits collagen expression in anti-Thymocyte Antibody-induced glomerulonephritis: Possible role of TGFβ. To test whether or not prostaglandins mediate extracellular matrix formation in immune-mediated glomerular disease, rats with anti-Thymocyte Antibody-induced glomerulonephritis were treated with prostaglandin E1 (PGE 1 ) (250 μ g/twice daily/s.c.). Glomerular expression of collagen types III and IV was assessed by Northern blotting, immunohistology and Western blotting. Proliferation of glomerular cells was evaluated by staining for the proliferating cell nuclear antigen (PCNA) and consecutive cell counting. At day five after induction of the disease, glomerular mRNA levels of collagen types III and IV were three- to fivefold higher compared with non-nephritic controls. Similarly glomerular deposition of these collagens was markedly increased when assessed by immunohistology. The treatment of nephritic rats with PGE 1 reduced the increased glomerular mRNA levels as well as the protein concentration and the deposition of extracellular collagens. The number of PCNA positive cells which was significantly higher in nephritic rats when compared with control animals (24 hr, nephritis 2.53 ± 0.33 and Control 0.26 ± 0.06, P = 0.011; 5 days, nephritis 5.10 ± 1.13 and Control 0.75 ± 0.08, cells per glomerular cross section, P = 0.03) was reduced by PGE 1 (24 hr, nephritis + PGE 1 0.44 ± 0.30, P=0.0001; 5 days, nephritis + PGE 1 1.91 ± 1.84 cells per glomerular cross section, P = 0.001). Prostaglandin E 1 also ameliorated the glomerular infiltration of monocytes at 24 hours (nephritis 4.36 ± 2.82, nephritis + PGE 1 2.20 ± 1.82, cells per glomerular cross section) and five days (nephritis 1.51 ± 0.58, nephritis + PGE 1 1.12 ± 0.61, cells per glomerular cross section). To further characterize possible mechanisms by which PGE 1 reduces extracellular matrix deposition, the glomerular expression of transforming growth factor (TGF- β ), and interleukin 1 β (IL-1 β ) was assessed by Northern blotting. Nephritic glomeruli showed increased mRNA levels of TGF- β at day 5 and IL-1 β at 24 hours when compared with control kidneys. Treatment of the animals with PGE 1 inhibited the mRNA expression of TGF- β and IL-1 β . These data demonstrate that PGE 1 reduces the glomerular expression of extracellular matrix proteins in anti-Thymocyte Antibody-induced glomerulonephritis, suggesting a beneficial role of prostaglandins in this proliferative glomerular immune injury. The effects of PGE 1 might be mediated by inhibition of TGF- β and IL-1 β production.

  • prostaglandin e1 reduces the glomerular mrna expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerular injury
    Journal of The American Society of Nephrology, 1996
    Co-Authors: Thomas Jocks, Friedrich Thaiss, Gunte Wolf, Gunthe Zahne, J Freudenberg, Udo Helmche, R A K Stahl
    Abstract:

    To study whether prostaglandins (PG) can regulate the mRNA expression of monocyte-chemoattractant protein 1 (MCP-1) in glomerular immune injury, MCP-1 mRNA levels were evaluated in anti-Thymocyte Antibody (ATS) -induced glomerular injury by Northern blotting and reverse transcription-polymerase chain reaction. Immune injury was induced in vivo by the intravenous application of ATS to male Wistar rats and in vitro by the perfusion of isolated rat kidneys with ATS and rat serum. In vivo 3 h and 5 days after Antibody application, glomerular mRNA expression of MCP-1 was markedly enhanced compared with controls. In the isolated perfused kidney, Antibody and complement also induced an increase in MCP-1 expression at 10 min and 60 min after Antibody perfusion. When the rats were treated with PGE (250 micrograms, twice daily), the increase in MCP-1 expression was reduced. This was associated with a reduction of intraglomerular recruitment of monocytes/macrophages. In the isolated perfused kidneys, PGE1 (1 mg/L) prevented the Antibody- and rat serum-stimulated increase in glomerular MCP-1 mRNA expression. These data demonstrate that PGE1 reduces glomerular MCP-1 mRNA expression in glomerulonephritis and in the isolated perfused rat kidney after induction of immune injury with Antibody and complement. The data suggest that prostaglandins might mediate MCP-1 effects in glomerular immune injuries.

Gunte Wolf - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin e1 inhibits collagen expression in anti Thymocyte Antibody induced glomerulonephritis possible role of tgfβ
    Kidney International, 1996
    Co-Authors: Andre Schneide, Friedrich Thaiss, Hanspete Rau, Gunte Wolf, Gunthe Zahne, Thomas Jocks
    Abstract:

    Prostaglandin E1 inhibits collagen expression in anti-Thymocyte Antibody-induced glomerulonephritis: Possible role of TGFβ. To test whether or not prostaglandins mediate extracellular matrix formation in immune-mediated glomerular disease, rats with anti-Thymocyte Antibody-induced glomerulonephritis were treated with prostaglandin E1 (PGE 1 ) (250 μ g/twice daily/s.c.). Glomerular expression of collagen types III and IV was assessed by Northern blotting, immunohistology and Western blotting. Proliferation of glomerular cells was evaluated by staining for the proliferating cell nuclear antigen (PCNA) and consecutive cell counting. At day five after induction of the disease, glomerular mRNA levels of collagen types III and IV were three- to fivefold higher compared with non-nephritic controls. Similarly glomerular deposition of these collagens was markedly increased when assessed by immunohistology. The treatment of nephritic rats with PGE 1 reduced the increased glomerular mRNA levels as well as the protein concentration and the deposition of extracellular collagens. The number of PCNA positive cells which was significantly higher in nephritic rats when compared with control animals (24 hr, nephritis 2.53 ± 0.33 and Control 0.26 ± 0.06, P = 0.011; 5 days, nephritis 5.10 ± 1.13 and Control 0.75 ± 0.08, cells per glomerular cross section, P = 0.03) was reduced by PGE 1 (24 hr, nephritis + PGE 1 0.44 ± 0.30, P=0.0001; 5 days, nephritis + PGE 1 1.91 ± 1.84 cells per glomerular cross section, P = 0.001). Prostaglandin E 1 also ameliorated the glomerular infiltration of monocytes at 24 hours (nephritis 4.36 ± 2.82, nephritis + PGE 1 2.20 ± 1.82, cells per glomerular cross section) and five days (nephritis 1.51 ± 0.58, nephritis + PGE 1 1.12 ± 0.61, cells per glomerular cross section). To further characterize possible mechanisms by which PGE 1 reduces extracellular matrix deposition, the glomerular expression of transforming growth factor (TGF- β ), and interleukin 1 β (IL-1 β ) was assessed by Northern blotting. Nephritic glomeruli showed increased mRNA levels of TGF- β at day 5 and IL-1 β at 24 hours when compared with control kidneys. Treatment of the animals with PGE 1 inhibited the mRNA expression of TGF- β and IL-1 β . These data demonstrate that PGE 1 reduces the glomerular expression of extracellular matrix proteins in anti-Thymocyte Antibody-induced glomerulonephritis, suggesting a beneficial role of prostaglandins in this proliferative glomerular immune injury. The effects of PGE 1 might be mediated by inhibition of TGF- β and IL-1 β production.

  • prostaglandin e1 reduces the glomerular mrna expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerular injury
    Journal of The American Society of Nephrology, 1996
    Co-Authors: Thomas Jocks, Friedrich Thaiss, Gunte Wolf, Gunthe Zahne, J Freudenberg, Udo Helmche, R A K Stahl
    Abstract:

    To study whether prostaglandins (PG) can regulate the mRNA expression of monocyte-chemoattractant protein 1 (MCP-1) in glomerular immune injury, MCP-1 mRNA levels were evaluated in anti-Thymocyte Antibody (ATS) -induced glomerular injury by Northern blotting and reverse transcription-polymerase chain reaction. Immune injury was induced in vivo by the intravenous application of ATS to male Wistar rats and in vitro by the perfusion of isolated rat kidneys with ATS and rat serum. In vivo 3 h and 5 days after Antibody application, glomerular mRNA expression of MCP-1 was markedly enhanced compared with controls. In the isolated perfused kidney, Antibody and complement also induced an increase in MCP-1 expression at 10 min and 60 min after Antibody perfusion. When the rats were treated with PGE (250 micrograms, twice daily), the increase in MCP-1 expression was reduced. This was associated with a reduction of intraglomerular recruitment of monocytes/macrophages. In the isolated perfused kidneys, PGE1 (1 mg/L) prevented the Antibody- and rat serum-stimulated increase in glomerular MCP-1 mRNA expression. These data demonstrate that PGE1 reduces glomerular MCP-1 mRNA expression in glomerulonephritis and in the isolated perfused rat kidney after induction of immune injury with Antibody and complement. The data suggest that prostaglandins might mediate MCP-1 effects in glomerular immune injuries.

Gunthe Zahne - One of the best experts on this subject based on the ideXlab platform.

  • prostaglandin e1 inhibits collagen expression in anti Thymocyte Antibody induced glomerulonephritis possible role of tgfβ
    Kidney International, 1996
    Co-Authors: Andre Schneide, Friedrich Thaiss, Hanspete Rau, Gunte Wolf, Gunthe Zahne, Thomas Jocks
    Abstract:

    Prostaglandin E1 inhibits collagen expression in anti-Thymocyte Antibody-induced glomerulonephritis: Possible role of TGFβ. To test whether or not prostaglandins mediate extracellular matrix formation in immune-mediated glomerular disease, rats with anti-Thymocyte Antibody-induced glomerulonephritis were treated with prostaglandin E1 (PGE 1 ) (250 μ g/twice daily/s.c.). Glomerular expression of collagen types III and IV was assessed by Northern blotting, immunohistology and Western blotting. Proliferation of glomerular cells was evaluated by staining for the proliferating cell nuclear antigen (PCNA) and consecutive cell counting. At day five after induction of the disease, glomerular mRNA levels of collagen types III and IV were three- to fivefold higher compared with non-nephritic controls. Similarly glomerular deposition of these collagens was markedly increased when assessed by immunohistology. The treatment of nephritic rats with PGE 1 reduced the increased glomerular mRNA levels as well as the protein concentration and the deposition of extracellular collagens. The number of PCNA positive cells which was significantly higher in nephritic rats when compared with control animals (24 hr, nephritis 2.53 ± 0.33 and Control 0.26 ± 0.06, P = 0.011; 5 days, nephritis 5.10 ± 1.13 and Control 0.75 ± 0.08, cells per glomerular cross section, P = 0.03) was reduced by PGE 1 (24 hr, nephritis + PGE 1 0.44 ± 0.30, P=0.0001; 5 days, nephritis + PGE 1 1.91 ± 1.84 cells per glomerular cross section, P = 0.001). Prostaglandin E 1 also ameliorated the glomerular infiltration of monocytes at 24 hours (nephritis 4.36 ± 2.82, nephritis + PGE 1 2.20 ± 1.82, cells per glomerular cross section) and five days (nephritis 1.51 ± 0.58, nephritis + PGE 1 1.12 ± 0.61, cells per glomerular cross section). To further characterize possible mechanisms by which PGE 1 reduces extracellular matrix deposition, the glomerular expression of transforming growth factor (TGF- β ), and interleukin 1 β (IL-1 β ) was assessed by Northern blotting. Nephritic glomeruli showed increased mRNA levels of TGF- β at day 5 and IL-1 β at 24 hours when compared with control kidneys. Treatment of the animals with PGE 1 inhibited the mRNA expression of TGF- β and IL-1 β . These data demonstrate that PGE 1 reduces the glomerular expression of extracellular matrix proteins in anti-Thymocyte Antibody-induced glomerulonephritis, suggesting a beneficial role of prostaglandins in this proliferative glomerular immune injury. The effects of PGE 1 might be mediated by inhibition of TGF- β and IL-1 β production.

  • prostaglandin e1 reduces the glomerular mrna expression of monocyte chemoattractant protein 1 in anti Thymocyte Antibody induced glomerular injury
    Journal of The American Society of Nephrology, 1996
    Co-Authors: Thomas Jocks, Friedrich Thaiss, Gunte Wolf, Gunthe Zahne, J Freudenberg, Udo Helmche, R A K Stahl
    Abstract:

    To study whether prostaglandins (PG) can regulate the mRNA expression of monocyte-chemoattractant protein 1 (MCP-1) in glomerular immune injury, MCP-1 mRNA levels were evaluated in anti-Thymocyte Antibody (ATS) -induced glomerular injury by Northern blotting and reverse transcription-polymerase chain reaction. Immune injury was induced in vivo by the intravenous application of ATS to male Wistar rats and in vitro by the perfusion of isolated rat kidneys with ATS and rat serum. In vivo 3 h and 5 days after Antibody application, glomerular mRNA expression of MCP-1 was markedly enhanced compared with controls. In the isolated perfused kidney, Antibody and complement also induced an increase in MCP-1 expression at 10 min and 60 min after Antibody perfusion. When the rats were treated with PGE (250 micrograms, twice daily), the increase in MCP-1 expression was reduced. This was associated with a reduction of intraglomerular recruitment of monocytes/macrophages. In the isolated perfused kidneys, PGE1 (1 mg/L) prevented the Antibody- and rat serum-stimulated increase in glomerular MCP-1 mRNA expression. These data demonstrate that PGE1 reduces glomerular MCP-1 mRNA expression in glomerulonephritis and in the isolated perfused rat kidney after induction of immune injury with Antibody and complement. The data suggest that prostaglandins might mediate MCP-1 effects in glomerular immune injuries.