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Journal: Skeletal Muscle
Article Title: Forskolin treatment enhances muscle regeneration and shows therapeutic potential with limitations in Duchenne muscular dystrophy
doi: 10.1186/s13395-025-00381-7
Figure Lengend Snippet: Morphological analysis of uninjured and injured muscles upon FSK treatments. A Scheme of FSK administration on DMD rats for a short (4-day) or long (12-day) treatment starting at 2 days post-injury (DPI). FSK was daily administered by IP injection at 25 mg/kg. B , C H&E (B) and SR (SR) on TA harvested at 14 DPI from WT, DMD, DMD treated with FSK short term (FSK S-T) or long term (FSK L–T). Scale bar 20 µm. D Quantification of SR positive area. E Quantification of the number of PDGFRa + cells per mm 2 . F – H Quantifications of FAP proliferation (F), Col I-Col III (G) and αSMA (H) positive area
Article Snippet: Cells were fixed with 4% PFA for 10 min at 4 °C and then permeabilized with 0.5% Triton X-100 for 10 min. After blocking with 5% bovine serum albumin (BSA), cells were incubated overnight at 4 °C with Collagen I-III (Abcam, ab34710) and
Techniques: Muscles, Injection
Journal: International Journal of Biological Sciences
Article Title: Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast
doi: 10.7150/ijbs.119129
Figure Lengend Snippet: Mice lacking Dectin-1 are protected from unilateral ureteric obstruction (UUO)-induced progressive renal fibrosis. Wild-type (WT) and Dectin-1 knockout (KO) mice challenged to sham or UUO operation. (A) Experimental design of the treatment procedure. (B) Representative photomicrographs illustrating H&E and Masson's trichrome staining in kidney tissues. Scale bar, 50 μm. (C) Representative photomicrographs illustrating immunohistochemical staining for fibronectin, collagen1, vimentin, and α-SMA in kidney tissues (n = 6 for each group). Scale bar, 50 μm. (D) Quantification of the positive staining area (%) in (C). (E) Representative western blot analysis of fibronectin, collagen1, vimentin, and α-SMA protein in the kidney tissues. α-Tubulin was used as loading control (n = 6 for each group). (F) Densitometric quantification of blots in (E). (G) Relative mRNA expression of Fn1 , Col1a1 , Vim , and Acta2 in kidney tissues (n = 6 for each group). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Article Snippet: Also,
Techniques: Knock-Out, Staining, Immunohistochemical staining, Western Blot, Control, Expressing
Journal: International Journal of Biological Sciences
Article Title: Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast
doi: 10.7150/ijbs.119129
Figure Lengend Snippet: Deletion of bone marrow (BM)-derived Dectin-1 inhibits unilateral ureteric obstruction (UUO)-induced renal fibrosis. (A) Experimental design of the treatment procedure. (B) Flow cytometric analysis showing the genetic background of CD45 alleles in the wild-type (WT) and Dectin-1 knockout (KO) mice. (C) Successful BM transplantations (BMTs) were confirmed by flow cytometric analysis of peripheral blood cells. (D-I) After successful BMT, mice from 4 groups (WT BM→WT, Dectin-1 KO BM→WT, WT BM→ Dectin-1 KO, and Dectin-1 KO BM→ Dectin-1 KO) were subjected to sham or UUO operation. (D) Representative photomicrographs illustrating H&E and Masson's trichrome staining in kidney tissues. Scale bar, 50 μm. (E) Representative photomicrographs illustrating immunohistochemical staining for fibronectin, collagen1, vimentin, and α-SMA in kidney tissues (n=3 for each group). Scale bar, 50 μm. (F) Quantification of the positive staining area (%) in (E). (G) Representative western blot analysis of fibronectin, collagen1, vimentin, and α-SMA protein in the kidney tissues. α-Tubulin was used as loading control (n = 3 for each group). (H) Densitometric quantification of blots in (G). (I) Relative mRNA expression of Fn1 , Col1a1 , Vim , and Acta2 in kidney tissues (n = 3 for each group). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Article Snippet: Also,
Techniques: Derivative Assay, Knock-Out, Staining, Immunohistochemical staining, Western Blot, Control, Expressing
Journal: International Journal of Biological Sciences
Article Title: Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast
doi: 10.7150/ijbs.119129
Figure Lengend Snippet: Macrophage-specific deletion of Dectin-1 protects against unilateral ureteric obstruction (UUO)-induced renal fibrosis. Dectin-1 f/f and Dectin-1 ΔCd68 mice challenged to sham or UUO operation. (A) Experimental design of the treatment procedure. (B) Representative photomicrographs illustrating H&E and Masson's trichrome staining in kidney tissues. Scale bar, 50 μm. (C) Representative photomicrographs illustrating immunohistochemical staining for fibronectin, collagen1, vimentin, and α-SMA in kidney tissues (n=6 for each group). Scale bar, 50 μm. (D) Quantification of the positive staining area (%) in (C). (E) Representative western blot analysis of fibronectin, collagen1, vimentin, and α-SMA protein in the kidney tissues. α-Tubulin was used as loading control (n = 6 for each group). (F) Densitometric quantification of blots in (E). (G) Relative mRNA expression of Fn1 , Col1a1 , Vim , and Acta2 in kidney tissues (n = 6 for each group). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Article Snippet: Also,
Techniques: Staining, Immunohistochemical staining, Western Blot, Control, Expressing
Journal: International Journal of Biological Sciences
Article Title: Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast
doi: 10.7150/ijbs.119129
Figure Lengend Snippet: Dectin-1 deficiency reduces macrophage-to-myofibroblast transition (MMT) through TGF-β/Smad pathway. Wild-type (WT) and Dectin-1 knockout (KO) mice subjected to unilateral ureteric obstruction (UUO) operation. (A) Representative flow cytometric images illustrating the expression of α-SMA + in CD45 + CD11b + F4/80 + live cells (left) and the percentage of α-SMA + cells in macrophages and its mean fluorescence intensity levels (2 parts in the right) in kidneys (n=6 for each group). (B) Relative mRNA expression of Acta2 in sorted macrophages from fibrotic kidneys (n = 5 for each group). (C) Schematic of Dectin-1 induced MMT. (D) Representative western blot analysis of TGF-β1 protein in the kidney tissues. α-Tubulin was used as loading control (n = 6 for each group). (E) Densitometric quantification of blots in (D). (F) Relative mRNA expression of Tgfb1 in kidney tissues (n = 5 for each group). (G) Relative mRNA expression of Tgfb1 in sorted macrophages from fibrotic kidneys (n = 5 for each group). (H) The concentrations of TGF-β1 detected by ELISA in supernatant from sorted macrophages of fibrotic kidneys (n = 5 for each group). (I) Representative flow cytometric images illustrating the expression of p-Smad2/3 + in CD45 + CD11b + F4/80 + live cells (left) and the percentage of p-Smad2/3 + cells in macrophages and its mean fluorescence intensity levels (2 parts in the right) in kidneys (n=6 for each group). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Article Snippet: Also,
Techniques: Knock-Out, Expressing, Fluorescence, Western Blot, Control, Enzyme-linked Immunosorbent Assay
Journal: International Journal of Biological Sciences
Article Title: Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast
doi: 10.7150/ijbs.119129
Figure Lengend Snippet: Inhibition of Dectin-1 attenuates chronic kidney disease (CKD) progression induced by unilateral ureteric obstruction (UUO) and ischemia-reperfusion (IR) in mice. (A-G) Laminarin was administered (300mg/kg/day) following sham or UUO surgery. (A) Experimental design of the treatment procedure. (B) Representative photomicrographs illustrating H&E and Masson's trichrome staining in kidney tissues. Scale bar, 50 μm. (C) Representative photomicrographs illustrating immunohistochemical staining for fibronectin, collagen1, vimentin, and α-SMA in kidney tissues (n=6 for each group). Scale bar, 50 μm. (D) Quantification of the positive staining area (%) in (C). (E) Representative western blot analysis of fibronectin, collagen1, vimentin, and α-SMA protein in the kidney tissues. GAPDH was used as loading control (n = 6 for each group). (F) Densitometric quantification of blots in (E). (G) Relative mRNA expression of Fn1 , Col1a1 , Vim , and Acta2 in kidney tissues (n = 6 for each group). (H-N) Laminarin was administered (300mg/kg/day) following sham or IR surgery. (H) Experimental design of the treatment procedure. (I) Representative photomicrographs illustrating H&E and Masson's trichrome staining in kidney tissues. Scale bar, 50 μm. (J) Representative photomicrographs illustrating immunohistochemical staining for fibronectin, collagen1, vimentin, and α-SMA in kidney tissues (n=6 for each group). Scale bar, 50 μm. (K) Quantification of the positive staining area (%) in (J). (L) Representative western blot analysis of fibronectin, collagen1, vimentin, and α-SMA protein in the kidney tissues. α-Tubulin was used as loading control (n = 6 for each group). (M) Densitometric quantification of blots in (L). (N) Relative mRNA expression of Fn1 , Col1a1 , Vim , and Acta2 in kidney tissues (n = 6 for each group). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Article Snippet: Also,
Techniques: Inhibition, Staining, Immunohistochemical staining, Western Blot, Control, Expressing