Periostin Regulates Goblet Cell Metaplasia in a Model of Allergic Airway Inflammation

Sehra, Sarita; Yao, Weiguo; Nguyen, Evelyn T.; Ahyi, Ayele Nati N.; Tuana, Florencia M. Barbé; Ahlfeld, Shawn K.; Snider, Paige; Tepper, Robert S.; Petrache, Irina; Conway, Simon J.; Kaplan, Mark H.

doi:10.4049/jimmunol.1002359

Cited by 66 publications

(68 citation statements)

References 54 publications

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“…IFN-γ-induced cell death involves STAT1-dependent translocation of Bax to the endoplasmic reticulum [58]. Sehra et al reported [59] that periostin, a 90-kDa member of the fasciclin-containing family and functions as part of the extracellular matrix, is expressed in a variety of tissues and expression is increased in airway epithelial cells from asthmatic patients as follows. Sensitization and challenge of periostin-deficient mice with OVA resulted in increased peripheral Th2 responses.…”

Section: Goblet Cell Metaplasia From Clara and Ciliated Cellsmentioning

confidence: 99%

Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma

Hayashi¹

2012

J Aller Ther

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Bronchial allergic asthma (asthma) is an airway inflammation characterized by airflow obstruction of variable degrees with bronchial hyper-responsiveness and is induced by a complex interaction of environmental and genetic factors. Asthma of the human can be divided into an immediate-and a late-phase reaction, and some of the patients develop a late-phase reaction after a symptom-free interval. Hallmarks of asthma are mucus overproduction by goblet cells associated with responses of helper T(Th)2 cells. Mucus hypersecretion from goblet cells themselves or by metaplasia and/or hyperplasia of goblet cells appears to be associated with disease severity in asthma, because mucus production by those cells in local bronchial-bronchiolar lesions causes airway mucus plugging. However, the mechanisms of mucus production are not fully understood. Molecular mechanisms of goblet cell metaplasia, differentiation and hyperplasia will be reviewed in this article. Also, the relationship between allergic inflammation in Th1/Th2 paradigm shift and thymic stromal lymphopoietin (TSLP) was included for the understanding of goblet cell response in asthma. The clarification of mechanisms of mucin production in vivo may lead to the development of novel therapeutic strategies to suppress mucus production in asthma.

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Section: Goblet Cell Metaplasia From Clara and Ciliated Cellsmentioning

confidence: 99%

Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma

Hayashi¹

2012

J Aller Ther

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“…POSTN has a characteristic structure ( Figure 1) consisting of four main domains, namely an N-terminus (encoded by exon 1) containing a signal peptide (SP), a cysteine-rich EMI domain (exons 2 and 3) made up of approximately 75 amino acids, and a tandem of four homologous FAS1 domains (exons [3][4][5][6][7][8][9][10][11][12][13][14]. The FAS1 domain is a structural homolog of an insect cell adhesion protein fasciclin I and acts as ligand for cell membrane integrins.…”

Section: Introductionmentioning

confidence: 99%

“…POSTN is a protein produced and secreted by the fibroblasts as a component of the extracellular matrix (ECM) where it is involved in regulating intercellular adhesion [3,4]. POSTN, originally named Osteoblast-Specific Factor 2 (OSF-2), was first identified in 1993 as a putative cell adhesion protein for preosteoblasts in a mouse osteoblastic MC3T3-E1 cell line [1,2,[4][5][6].…”

Section: Introductionmentioning

confidence: 99%

The role of periostin in neoplastic processes

Ratajczak‐Wielgomas

Dzięgiel

2015

Folia Histochem Cytobiol.

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Periostin, also called osteoblast-specific factor 2 (OSF-2), is a multifunctional glycoprotein that belongs to the group of matricellular proteins. Due to its characteristic molecular structure containing integrin-binding domains, periostin is capable of binding to multiple integrin receptors (avb3, avb5, a6b4), thus affecting the regulation of the intracellular signaling pathways associated with protein kinases PI3K/AKT and focal adhesion kinase (FAK). This protein thus plays a role in the adhesion process, in the migration of many cells, and importantly, epithelial-mesenchymal transition of cancer cells. Periostin also participates in the processes of angiogenesis and lymphangiogenesis, metastases of cancer cells, and remodeling of the extracellular matrix. Increased expression of periostin has been observed in various tumor types, including breast, NSCLC, colorectal, pancreatic, prostate, and ovarian cancers, as well as tumors of the head and neck, and glioblastomas. Many groups have recently reported on periostin's key role in tumor progression, which suggests that periostin can be considered a potential therapeutic target.

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“…Moreover, experimental studies have revealed that the lack of periostin induces a goblet cell hyperplasia in respiratory epithelium [34] and, consequently, a mucus hypersecretion. Thus, periostin may contribute to the enhancement of the mucus secretion in respiratory epithelium (Figure 1).…”

Section: Periostin and Bronchial Asthmamentioning

confidence: 99%

“…It is also involved in the regulation of mucus secretion performed by goblet cells of the respiratory bronchial epithelium, by inhibition Gob5 (putative calcium-activated chloride channel involved in the regulation of mucus production) expression and by binding to integrins α4 and β1/2 and induction of activation of intracellular pathways resulting in the reduction of the expression of transcription factors, such as NF-κB, Sp1, and AP-1 [34,35].…”

Section: Periostin and Bronchial Asthmamentioning

confidence: 99%

Periostin in bronchial asthma – a brief update

Grigoraș¹,

Lozneanu²,

Grigoraş³

et al. 2017

Arch Clin Cases

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Periostin is an extracellular matrix protein which intervenes in the regulation of angiogenesis, and in tumoral cells proliferation and invasion. Recent studies, mainly experimental models, have demonstrated the intervention of this molecule in asthmatic disease, by eosinophils recruitment, bronchial wall remodeling, and by stimulation of inflammatory cytokines production. Currently, periostin is considered a marker of type 2 inflammation in asthma, being secreted by respiratory epithelial cells triggered by IL-13 and IL-4. Concomitantly, periostin accumulated at the bronchial epithelial-connective tissue interface is involved in fibrogenesis and mucus secretion, in correlation with the intensity of bronchial mucosa eosinophilic inflammatory infiltrate. However, the intimate molecular mechanisms of periostin involvement in the pathogenic pathway of asthmatic diseases is far away from elucidation, further research being necessary to certify its value as a biomarker useful in diagnosis and in establishment of therapeutic schemes in bronchial asthma.

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Periostin Regulates Goblet Cell Metaplasia in a Model of Allergic Airway Inflammation

Cited by 66 publications

References 54 publications

Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma

Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma

The role of periostin in neoplastic processes

Periostin in bronchial asthma – a brief update

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