A critical role for Pin1 in allergic pulmonary eosinophilia in rats

Esnault, Stéphane; Rosenthal, Louis A.; Sedgwick, Julie B.; Szakaly, Renee J.; Sorkness, Ronald L.; Malter, James S.

doi:10.1016/j.jaci.2007.06.024

Cited by 37 publications

(50 citation statements)

References 35 publications

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“…2C). These results were consistent with the previous reports showing Pin1 inhibition selectively suppressed IFN-␥ expression in bronchoalveolar lavage cells (23,24). We then established Pin1-overexpressing human primary chondrocytes using ankle tissues obtained during surgery in an osteoarthritic patient.…”

Section: Role Of Pin1 In Proinflammatory Protein Expressionsupporting

confidence: 91%

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Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

Jeong

Pokharel

Lim

et al. 2009

The Journal of Immunology

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Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints and subsequent destruction of cartilage and bone. Inflammatory mediators such as PGs and proinflammatory cytokines contribute to RA progress. Pin1, a peptidyl prolyl isomerase, plays important pathophysiological roles in several diseases, including cancer and neurodegeneration. We found that both Pin1 and cyclooxygenase-2 (COX-2) were highly expressed in ankle tissues of type II collagen-induced RA mice. HTB-94 cells overexpressing Pin1 and primary cultured human chondrocytes showed increased basal expression of proinflammatory proteins (COX-2, inducible NO synthase, TNF-α, and IL-1β). Site-directed mutagenesis revealed that Pin1-mediated transcriptional activation of COX-2 was coordinately regulated by NF-κB, CREB, and C/EBP. Gel shift, reporter gene, and Western blot analyses confirmed that NF-κB, CREB, and C/EBP were consistently activated in chondrocytes overexpressing Pin1. Treatment of RA mice with juglone, a chemical inhibitor of Pin1, significantly reduced RA progress and COX-2 expression in the ankle tissues. Moreover, juglone dose dependently decreased the basal COX-2 expression in primary cultured chondrocytes from RA patients. These results demonstrate that Pin1 induction during RA progress stimulates proinflammatory protein expression by activating NF-κB, CREB, and C/EBP, and suggest that Pin1 is a potential therapeutic target of RA.

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Section: Role Of Pin1 In Proinflammatory Protein Expressionsupporting

confidence: 91%

“…Thus, MAPKs are not required for Pin1-mediated COX-2 expression. Abnormal Pin1 activity contributes to the pathogenesis of diverse diseases, including cancer, Alzheimer's disease, asthma, and allergies (24,46,47). We show in this study for the first time that Pin1 may also be a suitable target for RA.…”

Section: Discussionmentioning

confidence: 58%

Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

Jeong

Pokharel

Lim

et al. 2009

The Journal of Immunology

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“…We employed a known inhibitor of Pin1, juglone, to determine the neuroprotective efficacy of the compound in an established MPTP model of PD. Juglone (5-hydroxy-1,4-napthalenedione (C 10 H 6 O 3 )), an aromatic organic napthoquinone naturally found in the leaves, roots, and bark of black walnut plants, has been widely used as a Pin1 inhibitor (59,60). Juglone irreversibly inactivates enzymatic activity of human Pin1 by modification of thiol groups of cysteine residues (61).…”

Section: Discussionmentioning

confidence: 99%

“…Inhibition of Pin1 by juglone has shown anticancer effects in experimental models. Esnault et al (59) showed that juglone prevented acute and chronic rejection of MHC mismatched, orthotopic rat lung transplants by reducing the expression of IFN-␥ and CXCL-10 mRNA stability, accumulation, and protein expression after cell activation. Another report showed that juglone at a dose of 5 mg/kg can attenuate rheumatoid arthritis development and COX-2 expression in human primary cultured RA chondrocytes and in type II collagen (CII)-treated DBA/1J mice (60).…”

Section: Discussionmentioning

confidence: 99%

The Peptidyl-prolyl Isomerase Pin1 Up-regulation and Proapoptotic Function in Dopaminergic Neurons

Ghosh

Saminathan

Kanthasamy

et al. 2013

Journal of Biological Chemistry

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Background: Pin1 regulates several signaling proteins by isomerizing the cis/trans conformation of the Ser(P)-Pro peptide bond. Results: Pin1 is up-regulated in dopaminergic neurons in cell culture, animal models, and human PD brains. Pin1 inhibition protects dopaminergic neurons in PD models. Conclusion: Pin1 up-regulation plays a proapoptotic function in PD. Significance: Pin1 inhibition may be a viable translational strategy in PD.

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“…It was recently demonstrated that PIN1 may be a therapeutic target in the treatment or prevention of inflammatory disease. In vivo inhibition of PIN1 by juglone reduced eosinophilic pulmonary inflammation in rat asthma (Esnault et al 2007), rat allergic lung fibrosis (Shen et al 2008), kidney fibrosis in rat ureteral occlusion (Reese et al 2010), and inflammation in mice with type II collagen-induced rheumatoid arthritis (RA; Jeong HG et al 2009). In vitro inhibition of PIN1 by juglone and PIN1 small-interfering RNA (siRNA) blocked ultraviolet A radiation-stimulated COX-2 expression and PGE 2 production in mouse epidermal cells (Quyen et al 2013) and decreased COX-2 expression in primary cultured chondrocytes from RA patients (Jeong HG et al 2009).…”

Section: Introductionmentioning

confidence: 99%

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

et al. 2014

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Inflammatory responses and osteoclast differentiation play pivotal roles in the pathogenesis of osteolytic bone diseases such as periodontitis. Although overexpression or inhibition of peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (PIN1) offers a possible therapeutic strategy for chronic inflammatory diseases, the role of PIN1 in periodontal disease is unclear. The aim of the present study was to evaluate PIN1 expression in periodontitis patients as well as the effects of PIN1 inhibition by juglone or PIN1 small-interfering RNA (siRNA) and of PIN1 overexpression using a recombinant adenovirus encoding PIN1 (Ad-PIN1) on the inflammatory response and osteoclastic differentiation in lipopolysaccharide (LPS)-and nicotine-stimulated human periodontal ligament cells (PDLCs). PIN1 was up-regulated in chronically inflamed PDLCs from periodontitis patients and in LPS-and nicotine-exposed PDLCs. Inhibition of PIN1 by juglone or knockdown of PIN1 gene expression by siRNA markedly attenuated LPS-and nicotine-stimulated prostaglandin E 2 (PGE 2 ) and nitric oxide (NO) production, as well as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, whereas PIN1 overexpression by Ad-PIN1 increased it. LPS-and nicotine-induced nuclear factor (NF)-κB activation was blocked by juglone and PIN1 siRNA but increased by Ad-PIN1. Conditioned medium prepared from LPS-and nicotinetreated PDLCs increased the number of tartrate-resistant acid phosphatase-stained osteoclasts and osteoclast-specific gene expression. These responses were blocked by PIN1 inhibition and silencing but stimulated by Ad-PIN1. Furthermore, juglone and PIN1 siRNA inhibited LPS-and nicotine-induced osteoclastogenic cytokine expression in PDLCs. This study is the first to demonstrate that PIN1 inhibition exhibits anti-inflammatory effects and blocks osteoclastic differentiation in LPS-and nicotine-treated PDLCs. PIN1 inhibition may be a therapeutic strategy for inflammatory osteolysis in periodontal disease.

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A critical role for Pin1 in allergic pulmonary eosinophilia in rats

Cited by 37 publications

References 35 publications

Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

Novel Role of Pin1 Induction in Type II Collagen-Mediated Rheumatoid Arthritis

The Peptidyl-prolyl Isomerase Pin1 Up-regulation and Proapoptotic Function in Dopaminergic Neurons

PIN1 Inhibition Suppresses Osteoclast Differentiation and Inflammatory Responses

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