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Expression kinetics of <t>Ccn5</t> , Ccn2 , and Col Iα1 in isolated liver cells. ( A ) mRNA expression of Ccn5, Ccn2 , and Col Iα1 in hepatocytes, hepatic stellate cells (HSC), myofibroblasts (MFB) and portal myofibroblasts (pMF) in passage 2 (p2) cultured for the indicated time intervals was determined by RT-qPCR. Ccn5 and Col Iα1 expression is undetectable in hepatocytes, while in contrast Ccn2 mRNA increases during prolonged culture times in hepatocytes. In activated HSC and transdifferentiated MFB Ccn5 mRNA is up-regulated with the activation state of the cells. This up-regulation is even more pronounced than the expression of Ccn2 and parallels the induction of Col Iα1 in the course of HSC to MFB transition. Activated pMF displaying a MFB-like phenotype express large quantities of Ccn5 , Ccn2 , and Col Iα1 mRNAs. ( B ) Protein analysis confirms the absence of CCN5 in hepatocytes and the expression in HSC/MFB and PMF. In this analysis, Vimentin and α-SMA served as markers to demonstrate the mesenchymal phenotype of HSC, MFB and pMF. LCN2 was used as a marker for hepatocytes. Fibronectin and Col Iα1 expression confirmed elevated expression of extracellular matrix proteins during transition of HSC to MFB, while the discrimination between pMF and HSC/MFB was done by probing for Desmin

Ccn5 Wisp2, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ccn5 wisp2 - by Bioz Stars, 2026-05

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1) Product Images from "Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells"

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

Journal: Journal of Cell Communication and Signaling

doi: 10.1007/s12079-023-00757-8

Expression kinetics of Ccn5 , Ccn2 , and Col Iα1 in isolated liver cells. ( A ) mRNA expression of Ccn5, Ccn2 , and Col Iα1 in hepatocytes, hepatic stellate cells (HSC), myofibroblasts (MFB) and portal myofibroblasts (pMF) in passage 2 (p2) cultured for the indicated time intervals was determined by RT-qPCR. Ccn5 and Col Iα1 expression is undetectable in hepatocytes, while in contrast Ccn2 mRNA increases during prolonged culture times in hepatocytes. In activated HSC and transdifferentiated MFB Ccn5 mRNA is up-regulated with the activation state of the cells. This up-regulation is even more pronounced than the expression of Ccn2 and parallels the induction of Col Iα1 in the course of HSC to MFB transition. Activated pMF displaying a MFB-like phenotype express large quantities of Ccn5 , Ccn2 , and Col Iα1 mRNAs. ( B ) Protein analysis confirms the absence of CCN5 in hepatocytes and the expression in HSC/MFB and PMF. In this analysis, Vimentin and α-SMA served as markers to demonstrate the mesenchymal phenotype of HSC, MFB and pMF. LCN2 was used as a marker for hepatocytes. Fibronectin and Col Iα1 expression confirmed elevated expression of extracellular matrix proteins during transition of HSC to MFB, while the discrimination between pMF and HSC/MFB was done by probing for Desmin

Figure Legend Snippet: Expression kinetics of Ccn5 , Ccn2 , and Col Iα1 in isolated liver cells. ( A ) mRNA expression of Ccn5, Ccn2 , and Col Iα1 in hepatocytes, hepatic stellate cells (HSC), myofibroblasts (MFB) and portal myofibroblasts (pMF) in passage 2 (p2) cultured for the indicated time intervals was determined by RT-qPCR. Ccn5 and Col Iα1 expression is undetectable in hepatocytes, while in contrast Ccn2 mRNA increases during prolonged culture times in hepatocytes. In activated HSC and transdifferentiated MFB Ccn5 mRNA is up-regulated with the activation state of the cells. This up-regulation is even more pronounced than the expression of Ccn2 and parallels the induction of Col Iα1 in the course of HSC to MFB transition. Activated pMF displaying a MFB-like phenotype express large quantities of Ccn5 , Ccn2 , and Col Iα1 mRNAs. ( B ) Protein analysis confirms the absence of CCN5 in hepatocytes and the expression in HSC/MFB and PMF. In this analysis, Vimentin and α-SMA served as markers to demonstrate the mesenchymal phenotype of HSC, MFB and pMF. LCN2 was used as a marker for hepatocytes. Fibronectin and Col Iα1 expression confirmed elevated expression of extracellular matrix proteins during transition of HSC to MFB, while the discrimination between pMF and HSC/MFB was done by probing for Desmin

Techniques Used: Expressing, Isolation, Cell Culture, Quantitative RT-PCR, Activation Assay, Marker

Ccn5 expression in the inflammatory/fibrogenic bile duct obstruction model. ( A ) Mice were subjected to bile duct ligation (BDL) for 2 weeks. Hepatic expression of indicated genes was compared to sham-operated control animals by RT-qPCR showing that Col Iα1 , Acta2 , Lcn2 , and Tgfb1 are strongly upregulated during hepatic injury. Similarly, the expression of Ccn1 and Ccn2 in fibrotic liver tissue is increased, while the expression of Ccn3 is comparable in healthy and diseased livers. Interestingly, the expression of Ccn5 is significantly upregulated in diseased livers. Differences between the groups reaching significance are marked by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001). ( B ) Protein analysis confirms the increased expression of α-SMA and Col Iα1 and the elevated expression of CCN5 in livers of animals subjected to BDL. ( C ) Densitometric analysis of Western blot data depicted in ( B )

Figure Legend Snippet: Ccn5 expression in the inflammatory/fibrogenic bile duct obstruction model. ( A ) Mice were subjected to bile duct ligation (BDL) for 2 weeks. Hepatic expression of indicated genes was compared to sham-operated control animals by RT-qPCR showing that Col Iα1 , Acta2 , Lcn2 , and Tgfb1 are strongly upregulated during hepatic injury. Similarly, the expression of Ccn1 and Ccn2 in fibrotic liver tissue is increased, while the expression of Ccn3 is comparable in healthy and diseased livers. Interestingly, the expression of Ccn5 is significantly upregulated in diseased livers. Differences between the groups reaching significance are marked by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001). ( B ) Protein analysis confirms the increased expression of α-SMA and Col Iα1 and the elevated expression of CCN5 in livers of animals subjected to BDL. ( C ) Densitometric analysis of Western blot data depicted in ( B )

Techniques Used: Expressing, Ligation, Control, Quantitative RT-PCR, Western Blot

Effects of adenoviral overexpression of CCN5 in portal myofibroblasts. ( A ) Cultured portal myofibroblasts were infected for indicated time intervals with adenoviral expression vectors directing expression of murine CCN5, human CCN5 or Luciferase as a control. Mock infected cells served as a further control. Total RNA was isolated and the expression of mCcn5 , hccn5 , Col Iα1 , and Acta2 determined by RT-qPCR. ( B ) Protein analysis confirms the prominent overexpression of the transgenes (CCN5, Luciferase). Both CCN5 transgenes cause a reduction in Col Iα1 expression after infection for 48 h, 72 h, and 96 h, as evaluated by densitometric analysis of the depicted Western blot results. On the other hand, the effect on α-SMA expression is much less, leading to a lower expression only at 72 h and 96 h. ( C ) Western blot analysis demonstrates that overexpression of CCN5 results in reduced expression of the TGF-β type I receptor (ALK5, TβRI) and TGF-β type II receptor (TβRII). As a mutual consequence of the lowered receptor expression, Smad2 gets less activated from 48 h on, while at 72 h and 96 h after overexpression of CCN5 the genuine BMP or „alternative “ TGF-β1/Smad pathway as assessed by increased Smad1/5/8 phosphorylation is activated. In addition, Jun B is strongly up-regulated in cells overexpressing CCN5. GAPDH expression was used in Western blot analysis to document equal protein loading. Depicted is a representative experiment of an analysis that was done twice. The densitometric analysis of the Western blot is shown in Suppl. Figure 6

Figure Legend Snippet: Effects of adenoviral overexpression of CCN5 in portal myofibroblasts. ( A ) Cultured portal myofibroblasts were infected for indicated time intervals with adenoviral expression vectors directing expression of murine CCN5, human CCN5 or Luciferase as a control. Mock infected cells served as a further control. Total RNA was isolated and the expression of mCcn5 , hccn5 , Col Iα1 , and Acta2 determined by RT-qPCR. ( B ) Protein analysis confirms the prominent overexpression of the transgenes (CCN5, Luciferase). Both CCN5 transgenes cause a reduction in Col Iα1 expression after infection for 48 h, 72 h, and 96 h, as evaluated by densitometric analysis of the depicted Western blot results. On the other hand, the effect on α-SMA expression is much less, leading to a lower expression only at 72 h and 96 h. ( C ) Western blot analysis demonstrates that overexpression of CCN5 results in reduced expression of the TGF-β type I receptor (ALK5, TβRI) and TGF-β type II receptor (TβRII). As a mutual consequence of the lowered receptor expression, Smad2 gets less activated from 48 h on, while at 72 h and 96 h after overexpression of CCN5 the genuine BMP or „alternative “ TGF-β1/Smad pathway as assessed by increased Smad1/5/8 phosphorylation is activated. In addition, Jun B is strongly up-regulated in cells overexpressing CCN5. GAPDH expression was used in Western blot analysis to document equal protein loading. Depicted is a representative experiment of an analysis that was done twice. The densitometric analysis of the Western blot is shown in Suppl. Figure 6

Techniques Used: Over Expression, Cell Culture, Infection, Expressing, Luciferase, Control, Isolation, Quantitative RT-PCR, Western Blot

Impact of CCN5 on TGF-β signaling. Portal myofibroblasts were infected with adenoviral vectors expressing either human CCN5 (hCCN5) or the luciferase reporter gene (Luc). After 48 h, the cells were stimulated with the indicated concentrations of recombinant TGF-β1. Protein extracts and supernatants were prepared and tested for expression of Col Iα1, Fibronectin, α-SMA, CHOP, GAPDH ( left panel, cell lysate ), Col Iα1, Fibronectin, hCCN5 ( middle panel, culture supernatant ), and GRP94, GRP78, CCN2, and CCN5 ( right panel, cell lysate ). The expression of β-actin was used to document equal protein loading in each lane. Of note, there was no significant effect on the extracellular matrix components Col Iα1, Fibronectin and the activation marker α-SMA, but a strong TGF-β1 independent up-regulation of the UPR related proteins GRP94, GRP78 and CHOP. The densitometric analysis of the three Western blots is shown in Suppl. Figure 7

Figure Legend Snippet: Impact of CCN5 on TGF-β signaling. Portal myofibroblasts were infected with adenoviral vectors expressing either human CCN5 (hCCN5) or the luciferase reporter gene (Luc). After 48 h, the cells were stimulated with the indicated concentrations of recombinant TGF-β1. Protein extracts and supernatants were prepared and tested for expression of Col Iα1, Fibronectin, α-SMA, CHOP, GAPDH ( left panel, cell lysate ), Col Iα1, Fibronectin, hCCN5 ( middle panel, culture supernatant ), and GRP94, GRP78, CCN2, and CCN5 ( right panel, cell lysate ). The expression of β-actin was used to document equal protein loading in each lane. Of note, there was no significant effect on the extracellular matrix components Col Iα1, Fibronectin and the activation marker α-SMA, but a strong TGF-β1 independent up-regulation of the UPR related proteins GRP94, GRP78 and CHOP. The densitometric analysis of the three Western blots is shown in Suppl. Figure 7

Techniques Used: Infection, Expressing, Luciferase, Recombinant, Activation Assay, Marker, Western Blot

CCN5 induces endoplasmic reticulum stress in portal myofibroblasts. ( A ) Portal myofibroblasts were infected with indicated adenoviral constructs for indicated time intervals. Subsequently, total RNA was isolated, cDNA synthesized. The expression of unspliced (u) and spliced (s) Xbp1 expression after infection with adenoviral vectors expressing murine or human CCN5 was analyzed by semi-quantitative PCR. Spliced Xbp1 (Xbp1 (s)) transcripts were found in the presence of overexpressed mCCN5 and hCCN5, while cells that were infected with a control virus (Ad-Luc) or cells that were left uninfected showed no spliced Xbp1 . In this analysis, GAPDH was taken as a loading control. ( B ) Relative mRNA expression of Grp94 , Bip and Chop as assessed by RT-qPCR in samples taken from ( A ). ( C ) Western blot analysis of GRP94, GRP78/BIP, IRE1α, ATF6, peIF2α, eIF2α, ATF4, CHOP, pJNK, JNK2, cytochrome c, cleaved caspase-9, and cleaved caspase-3 in protein samples taken from portal myofibroblasts that were infected with indicated adenoviral vectors for indicated time intervals. Expression of GAPDH was used to demonstrate equal protein loading in each lane. The densitometric analysis of the Western blot is given in Suppl. Figure 8

Figure Legend Snippet: CCN5 induces endoplasmic reticulum stress in portal myofibroblasts. ( A ) Portal myofibroblasts were infected with indicated adenoviral constructs for indicated time intervals. Subsequently, total RNA was isolated, cDNA synthesized. The expression of unspliced (u) and spliced (s) Xbp1 expression after infection with adenoviral vectors expressing murine or human CCN5 was analyzed by semi-quantitative PCR. Spliced Xbp1 (Xbp1 (s)) transcripts were found in the presence of overexpressed mCCN5 and hCCN5, while cells that were infected with a control virus (Ad-Luc) or cells that were left uninfected showed no spliced Xbp1 . In this analysis, GAPDH was taken as a loading control. ( B ) Relative mRNA expression of Grp94 , Bip and Chop as assessed by RT-qPCR in samples taken from ( A ). ( C ) Western blot analysis of GRP94, GRP78/BIP, IRE1α, ATF6, peIF2α, eIF2α, ATF4, CHOP, pJNK, JNK2, cytochrome c, cleaved caspase-9, and cleaved caspase-3 in protein samples taken from portal myofibroblasts that were infected with indicated adenoviral vectors for indicated time intervals. Expression of GAPDH was used to demonstrate equal protein loading in each lane. The densitometric analysis of the Western blot is given in Suppl. Figure 8

Techniques Used: Infection, Construct, Isolation, Synthesized, Expressing, Real-time Polymerase Chain Reaction, Control, Virus, Quantitative RT-PCR, Western Blot

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Journal: Journal of Cell Communication and Signaling

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

doi: 10.1007/s12079-023-00757-8

Figure Lengend Snippet: Expression kinetics of Ccn5 , Ccn2 , and Col Iα1 in isolated liver cells. ( A ) mRNA expression of Ccn5, Ccn2 , and Col Iα1 in hepatocytes, hepatic stellate cells (HSC), myofibroblasts (MFB) and portal myofibroblasts (pMF) in passage 2 (p2) cultured for the indicated time intervals was determined by RT-qPCR. Ccn5 and Col Iα1 expression is undetectable in hepatocytes, while in contrast Ccn2 mRNA increases during prolonged culture times in hepatocytes. In activated HSC and transdifferentiated MFB Ccn5 mRNA is up-regulated with the activation state of the cells. This up-regulation is even more pronounced than the expression of Ccn2 and parallels the induction of Col Iα1 in the course of HSC to MFB transition. Activated pMF displaying a MFB-like phenotype express large quantities of Ccn5 , Ccn2 , and Col Iα1 mRNAs. ( B ) Protein analysis confirms the absence of CCN5 in hepatocytes and the expression in HSC/MFB and PMF. In this analysis, Vimentin and α-SMA served as markers to demonstrate the mesenchymal phenotype of HSC, MFB and pMF. LCN2 was used as a marker for hepatocytes. Fibronectin and Col Iα1 expression confirmed elevated expression of extracellular matrix proteins during transition of HSC to MFB, while the discrimination between pMF and HSC/MFB was done by probing for Desmin

Article Snippet: The two expression vectors RC204636 and MR203197 encoding full-length human or mouse Myc-DDK-tagged CCN5/WISP2 were obtained from Origene.

Techniques: Expressing, Isolation, Cell Culture, Quantitative RT-PCR, Activation Assay, Marker

Journal: Journal of Cell Communication and Signaling

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

doi: 10.1007/s12079-023-00757-8

Figure Lengend Snippet: Ccn5 expression in the inflammatory/fibrogenic bile duct obstruction model. ( A ) Mice were subjected to bile duct ligation (BDL) for 2 weeks. Hepatic expression of indicated genes was compared to sham-operated control animals by RT-qPCR showing that Col Iα1 , Acta2 , Lcn2 , and Tgfb1 are strongly upregulated during hepatic injury. Similarly, the expression of Ccn1 and Ccn2 in fibrotic liver tissue is increased, while the expression of Ccn3 is comparable in healthy and diseased livers. Interestingly, the expression of Ccn5 is significantly upregulated in diseased livers. Differences between the groups reaching significance are marked by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001). ( B ) Protein analysis confirms the increased expression of α-SMA and Col Iα1 and the elevated expression of CCN5 in livers of animals subjected to BDL. ( C ) Densitometric analysis of Western blot data depicted in ( B )

Article Snippet: The two expression vectors RC204636 and MR203197 encoding full-length human or mouse Myc-DDK-tagged CCN5/WISP2 were obtained from Origene.

Techniques: Expressing, Ligation, Control, Quantitative RT-PCR, Western Blot

Journal: Journal of Cell Communication and Signaling

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

doi: 10.1007/s12079-023-00757-8

Figure Lengend Snippet: Effects of adenoviral overexpression of CCN5 in portal myofibroblasts. ( A ) Cultured portal myofibroblasts were infected for indicated time intervals with adenoviral expression vectors directing expression of murine CCN5, human CCN5 or Luciferase as a control. Mock infected cells served as a further control. Total RNA was isolated and the expression of mCcn5 , hccn5 , Col Iα1 , and Acta2 determined by RT-qPCR. ( B ) Protein analysis confirms the prominent overexpression of the transgenes (CCN5, Luciferase). Both CCN5 transgenes cause a reduction in Col Iα1 expression after infection for 48 h, 72 h, and 96 h, as evaluated by densitometric analysis of the depicted Western blot results. On the other hand, the effect on α-SMA expression is much less, leading to a lower expression only at 72 h and 96 h. ( C ) Western blot analysis demonstrates that overexpression of CCN5 results in reduced expression of the TGF-β type I receptor (ALK5, TβRI) and TGF-β type II receptor (TβRII). As a mutual consequence of the lowered receptor expression, Smad2 gets less activated from 48 h on, while at 72 h and 96 h after overexpression of CCN5 the genuine BMP or „alternative “ TGF-β1/Smad pathway as assessed by increased Smad1/5/8 phosphorylation is activated. In addition, Jun B is strongly up-regulated in cells overexpressing CCN5. GAPDH expression was used in Western blot analysis to document equal protein loading. Depicted is a representative experiment of an analysis that was done twice. The densitometric analysis of the Western blot is shown in Suppl. Figure 6

Article Snippet: The two expression vectors RC204636 and MR203197 encoding full-length human or mouse Myc-DDK-tagged CCN5/WISP2 were obtained from Origene.

Techniques: Over Expression, Cell Culture, Infection, Expressing, Luciferase, Control, Isolation, Quantitative RT-PCR, Western Blot

Journal: Journal of Cell Communication and Signaling

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

doi: 10.1007/s12079-023-00757-8

Figure Lengend Snippet: Impact of CCN5 on TGF-β signaling. Portal myofibroblasts were infected with adenoviral vectors expressing either human CCN5 (hCCN5) or the luciferase reporter gene (Luc). After 48 h, the cells were stimulated with the indicated concentrations of recombinant TGF-β1. Protein extracts and supernatants were prepared and tested for expression of Col Iα1, Fibronectin, α-SMA, CHOP, GAPDH ( left panel, cell lysate ), Col Iα1, Fibronectin, hCCN5 ( middle panel, culture supernatant ), and GRP94, GRP78, CCN2, and CCN5 ( right panel, cell lysate ). The expression of β-actin was used to document equal protein loading in each lane. Of note, there was no significant effect on the extracellular matrix components Col Iα1, Fibronectin and the activation marker α-SMA, but a strong TGF-β1 independent up-regulation of the UPR related proteins GRP94, GRP78 and CHOP. The densitometric analysis of the three Western blots is shown in Suppl. Figure 7

Article Snippet: The two expression vectors RC204636 and MR203197 encoding full-length human or mouse Myc-DDK-tagged CCN5/WISP2 were obtained from Origene.

Techniques: Infection, Expressing, Luciferase, Recombinant, Activation Assay, Marker, Western Blot

Journal: Journal of Cell Communication and Signaling

Article Title: Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells

doi: 10.1007/s12079-023-00757-8

Figure Lengend Snippet: CCN5 induces endoplasmic reticulum stress in portal myofibroblasts. ( A ) Portal myofibroblasts were infected with indicated adenoviral constructs for indicated time intervals. Subsequently, total RNA was isolated, cDNA synthesized. The expression of unspliced (u) and spliced (s) Xbp1 expression after infection with adenoviral vectors expressing murine or human CCN5 was analyzed by semi-quantitative PCR. Spliced Xbp1 (Xbp1 (s)) transcripts were found in the presence of overexpressed mCCN5 and hCCN5, while cells that were infected with a control virus (Ad-Luc) or cells that were left uninfected showed no spliced Xbp1 . In this analysis, GAPDH was taken as a loading control. ( B ) Relative mRNA expression of Grp94 , Bip and Chop as assessed by RT-qPCR in samples taken from ( A ). ( C ) Western blot analysis of GRP94, GRP78/BIP, IRE1α, ATF6, peIF2α, eIF2α, ATF4, CHOP, pJNK, JNK2, cytochrome c, cleaved caspase-9, and cleaved caspase-3 in protein samples taken from portal myofibroblasts that were infected with indicated adenoviral vectors for indicated time intervals. Expression of GAPDH was used to demonstrate equal protein loading in each lane. The densitometric analysis of the Western blot is given in Suppl. Figure 8

Article Snippet: The two expression vectors RC204636 and MR203197 encoding full-length human or mouse Myc-DDK-tagged CCN5/WISP2 were obtained from Origene.

Techniques: Infection, Construct, Isolation, Synthesized, Expressing, Real-time Polymerase Chain Reaction, Control, Virus, Quantitative RT-PCR, Western Blot

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