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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and <t>p</t> <t>-JNK</t> in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).
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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and <t>p</t> <t>-JNK</t> in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).
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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and <t>p</t> <t>-JNK</t> in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).
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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and <t>p</t> <t>-JNK</t> in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).
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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and <t>p</t> <t>-JNK</t> in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).
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Immunohistochemical analysis of β-catenin, p -SMAD2/3, and p -JNK in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).

Journal: Regenerative Therapy

Article Title: Role of WIF-1 in regulating chondrocyte dedifferentiation and matrix production through WNT pathway

doi: 10.1016/j.reth.2026.101083

Figure Lengend Snippet: Immunohistochemical analysis of β-catenin, p -SMAD2/3, and p -JNK in early-passage, late-passage, WIF1-silenced, and WIF1-overexpressing human auricular chondrocytes. (a–c) IHC staining of β-catenin, p -SMAD2/3, and p -JNK in early-passage (P2) and late-passage (P7) chondrocyte pellets. (d–f) IHC staining of the same markers in P2 chondrocytes transduced with scramble shRNA or shWIF1, and in P7 pellets transduced with Empty control or WIF1 overexpression lentivirus. (e, g, i) High-magnification views corresponding to β-catenin, p -SMAD2/3, and p -JNK staining in control versus WIF1-modulated groups. Scale bars: 100 μm (low magnification), 20 μm (high magnification).

Article Snippet: p -JNK , Bioss , bs-1640R , Polyclonal , 1:200 , IHC.

Techniques: Immunohistochemical staining, Immunohistochemistry, Transduction, shRNA, Control, Over Expression, Staining