Results: 5

1.
Fig 5.

Fig 5. From: Proliferative action of mast-cell tryptase is mediated by PAR2, COX2, prostaglandins, and PPAR?: Possible relevance to human fibrotic disorders.

PPARγ expression in human testes. (a) RT-PCR analysis showing PPARγ mRNA expression in testicular biopsies from patients with normal spermatogenesis and GA, SCO, and MA syndromes. (b) A hematoxylin-stained human testicular biopsy after LCM of the wall of the seminiferous tubules. Material obtained was used for RT-PCR analysis. T, seminiferous tubule. (Bar, 20 μm.) (c) RT-PCR analysis indicating PPARγ mRNA expression in a sample of testicular tubular wall obtained by LCM and LPC. Note that PPARγ mRNA was detected in samples of all biopsies (normal group, n = 7; SCO syndrome, n = 7; GA syndrome, n = 9; and MA syndrome, n = 6).

Mónica B. Frungieri, et al. Proc Natl Acad Sci U S A. 2002 November 12;99(23):15072-15077.
2.
Fig 4.

Fig 4. From: Proliferative action of mast-cell tryptase is mediated by PAR2, COX2, prostaglandins, and PPAR?: Possible relevance to human fibrotic disorders.

COX2 expression in human testes with fibrotic changes. (a) RT-PCR analysis showing COX2 mRNA expression in testicular biopsies from patients with GA, SCO, and MA syndromes. COX2 was not found in normal testicular biopsies. Normal group, n = 7; SCO syndrome, n = 7; GA syndrome, n = 9; and MA syndrome, n = 6. First lane, size markers. (bd) Immunohistochemical staining showing COX2 expression in testicular biopsies. (b) COX2 in a testicular biopsy from a patient with GA syndrome. (c) COX2 immunostaining is not detected in a control section in which the COX2 antiserum was replaced by normal rabbit serum. (d) COX2 was not observed in biopsies from men showing normal spermatogenesis. Asterisks indicate the interstitial compartment. (Bar, 100 μm.) Note that COX2 RNA expression and specific immunoreaction were not found in normal testicular biopsies (normal group, n = 7), whereas COX2 was detected in all pathological samples examined (SCO syndrome, n = 7; GA syndrome, n = 9; and MA syndrome, n = 6).

Mónica B. Frungieri, et al. Proc Natl Acad Sci U S A. 2002 November 12;99(23):15072-15077.
3.
Fig 3.

Fig 3. From: Proliferative action of mast-cell tryptase is mediated by PAR2, COX2, prostaglandins, and PPAR?: Possible relevance to human fibrotic disorders.

Identification of tryptase-positive mast cells and PAR2 in human testes with fibrotic changes. (a) Immunohistochemical staining of tryptase-containing mast cells in the interstitium and the wall of the seminiferous tubules (arrows) in a human testicular biopsy from a patient showing subnormal spermatogenesis and tubular fibrosis. For complete and detailed quantitative evaluation of the observed changes, see ref. 18. (Bar, 60 μm.) (b) RT-PCR analysis showing PAR2 mRNA expression in human testes. (cf) Immunohistochemical staining showing PAR2 expression. PAR2 in a human testicular biopsy from a patient with SCO syndrome in interstitial cells (arrow) and the germinal epithelium (asterisk) (c). In a consecutive section, the PAR2 antibody was incubated previously with a specific blocking peptide to show specificity (d). For control purposes, the PAR2 antiserum was replaced by normal goat serum (e) and PBS buffer (f). (Bar, 30 μm.) Note that PAR2 RNA expression and specific immunoreaction were detected in all biopsies examined (normal group, n = 7; SCO syndrome, n = 7; GA syndrome, n = 9; and MA syndrome, n = 6).

Mónica B. Frungieri, et al. Proc Natl Acad Sci U S A. 2002 November 12;99(23):15072-15077.
4.
Fig 2.

Fig 2. From: Proliferative action of mast-cell tryptase is mediated by PAR2, COX2, prostaglandins, and PPAR?: Possible relevance to human fibrotic disorders.

Tryptase and the PAR2 agonist peptide SLIGKV stimulate fibroblast proliferation indirectly via 15d-PGJ2 and PPARγ. (a) PGJ2 and its metabolite 15d-PGJ2 stimulate HFFF2 proliferation, whereas PGs D2, E1, E2, and F have no effect. BADGE (a PPARγ antagonist) blocks the stimulatory action of recombinant human tryptase, PAR2 agonist peptide SLIGKV, PGJ2, and 15d-PGJ2 on HFFF2 proliferation. This figure shows results obtained from one of three experiments that yielded comparable results. The results shown are means + SEMs of n = 8–24 replicate wells per treatment. *, P < 0.05 vs. the corresponding control group. mIU, milliunits. (b) RT-PCR analysis showing PPARγ mRNA expression in HFFF2 cells (Left). (Right) Size markers. (c and d) Immunofluorescence staining showing PPARγ expression in the nucleus of HFFF2 cells (c). PPARγ immunostaining is not detected in a control section, in which the PPARγ antibody was replaced by normal nonimmune mouse serum (d). (Bar, 40 μm.) (eg) Immunocytochemical staining of the proliferation marker proliferating cell nuclear antigen. After treatment with 15d-PGJ2 (f) and tryptase (g), more nuclei of HFFF2 cells are immunoreactive compared with basal conditions (e). (Bar, 40 μm.)

Mónica B. Frungieri, et al. Proc Natl Acad Sci U S A. 2002 November 12;99(23):15072-15077.
5.
Fig 1.

Fig 1. From: Proliferative action of mast-cell tryptase is mediated by PAR2, COX2, prostaglandins, and PPAR?: Possible relevance to human fibrotic disorders.

Trypase via PAR2 increases COX2 levels and stimulates PG synthesis and fibroblast proliferation. (a) Example of an RT-PCR analysis, showing rapid up-regulation of COX2 mRNA in HFFF2 cells after treatment with tryptase. mIU, milliunits. (b) Immunoblot depicting increased COX2 protein levels in HFFF2 cells from 10 to 1,440 min after treatment with tryptase (2.5 μg of total protein per lane). (c) Immunoblot showing that the PAR2 agonist peptide SLIGKV also increases COX2 protein levels (15 μg of total protein per lane). (d) HMCs (HMC-1) contain tryptase (see Western blot, Left, 15 μg of total protein). Dot blot shows that HMC-1 cells contain tryptase and secrete tryptase into the culture medium (Right, basal or HMC-1-conditioned medium, collected from 5 × 106 cells after 24 h of incubation, were loaded). (e and f) Tryptase increases PGF (e) and 15d-PGJ2 (f) production in HFFF2s. The data represent means ± SEMs of values obtained after 1 and 3 h of treatment with tryptase (n = 4 per treatment). *, P < 0.05 vs. the corresponding control group. (g) Tryptase stimulates fibroblast proliferation via PAR2, COX2 up-regulation, and PGJ2 production. Meloxicam (a COX2 antagonist) inhibits the stimulatory action of conditioned medium collected from HMCs (HMC-1), recombinant human tryptase, and the PAR2 agonist peptide SLIGKV on HFFF2 proliferation after 24 h of incubation. This figure shows results obtained from one of three experiments that yielded comparable results. The results shown are means + SEMs of n = 8–12 replicate wells per treatment. *, P < 0.05 vs. the corresponding control group.

Mónica B. Frungieri, et al. Proc Natl Acad Sci U S A. 2002 November 12;99(23):15072-15077.

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