S100A7: A rAMPing up AMP molecule in psoriasis

D’Amico, Fabio; Skarmoutsou, Evangelia; Granata, Mariagrazia; Trovato, Chiara Maria; Rossi, Giulio A.; Mazzarino, María Clorinda

doi:10.1016/j.cytogfr.2016.01.002

Cited by 41 publications

(35 citation statements)

References 101 publications

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“…An increased mRNA expression of S100A7 was also detected in the dental pulp tissue obtained from orthodontically moved teeth, suggesting it also plays a role in vivo. S100A7 is a relatively small calcium‐binding protein, which is abundantly expressed in inflamed skin, such as psoriatic lesion, and in a tumor microenvironment (D'Amico et al, ; Emberley, Murphy, & Watson, ). Expression of S100A7 in tissues is upregulated in response to pro‐inflammatory cytokines, such as IL‐1, IL‐6, IL‐17, and IL‐22 (D'Amico et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…S100A7 is a relatively small calcium‐binding protein, which is abundantly expressed in inflamed skin, such as psoriatic lesion, and in a tumor microenvironment (D'Amico et al, ; Emberley, Murphy, & Watson, ). Expression of S100A7 in tissues is upregulated in response to pro‐inflammatory cytokines, such as IL‐1, IL‐6, IL‐17, and IL‐22 (D'Amico et al, ). We also observed that HPDCs treated with IL‐1 showed an increased production of S100A7 (Figure a).…”

Section: Discussionmentioning

confidence: 99%

“…We also observed that HPDCs treated with IL‐1 showed an increased production of S100A7 (Figure a). S100A7 performs important extracellular functions, and it can act as a chemokine and cytokine playing a pivotal role in the promotion and exacerbation of inflammatory responses (D'Amico et al, ; Jinquan et al, ).…”

Section: Discussionmentioning

confidence: 99%

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Mechanical stress induced S100A7 expression in human dental pulp cells to augment osteoclast differentiation

et al. 2019

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Objectives: Mechanical injury of dental pulp leads to root resorption by osteoclasts/ odontoclasts. S100 proteins have been demonstrated to be involved in inflammatory processes and bone remodeling. This study aimed to investigate the effect of mechanical stress on S100A7 expression by human dental pulp cells (HDPCs) and the effect of S100A7 proteins on osteoclast differentiation. Materials and Methods: Isolated HDPCs were stimulated with compressive loading(2 and 6 hr), or shear loading (2, 6, and 16 hr). S100 mRNA expression and S100A7 protein levels were determined by real-time PCR and ELISA, respectively. Osteoclast differentiation was analyzed using primary human monocytes. The differentiation and activity of osteoclasts were examined by TRAcP staining and dentine resorption.In addition, the expression of S100A7 was analyzed in pulp tissues obtained from orthodontically treated teeth. Results:Compressive and shear mechanical stress significantly upregulated both mRNA and protein level of S100A7. Dental pulp tissues from orthodontically treated teeth exhibited higher S100A7 mRNA levels compared to non-treated control teeth. S100A7 promoted osteoclast differentiation by primary human monocytes.Moreover, S100A7 significantly enhanced dentine resorption by these cells. Conclusions:Mechanical stress induced expression of S100A7 by human dental pulp cells and this may promote root resorption by inducing osteoclast differentiation and activity. K E Y W O R D Sdental pulp, inflammation, mechanical stress, Osteoclast, S100 protein, S100A7 | 813 CHAROENPONG Et Al.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Mechanical stress induced S100A7 expression in human dental pulp cells to augment osteoclast differentiation

et al. 2019

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“…Increasing evidence suggests that hS100A7 plays critical roles in amplifying the inflammatory process in psoriatic skin, perpetuating the disease phenotype. [42, 43] In human cultured keratinocytes, hS100A7 also induce the expression of several differentiation markers, which are overexpressed in psoriatic skin. [44, 45] In our study, we confirmed that mS100a7a15 was overexpressed in psoriasis model skin.…”

Section: Discussionmentioning

confidence: 99%

Human S100A7 Induces Mature Interleukin1α Expression by RAGE-p38 MAPK-Calpain1 Pathway in Psoriasis

Jing

et al. 2017

PLoS ONE

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Psoriatic keratinocytes express exaggerated levels of inflammatory cytokines, and show aberrant hyperproliferation and terminal differentiation in the pathogenesis of psoriasis. The antimicrobial protein hS100A7 (psoriasin) has been found highly expressed in psoriatic skin, but the mechanism and physiological function remain largely unknown. We observed that hS100A7 induces mature interleukin 1α (17kDa) expression in normal human epidermal keratinocytes, which is dependent on RAGE-p38 MAPK and calpain-1 as the inhibitors or knockdown of them completely decreased the expression of mature interleukin1α. Then, we proved mS100a7a15, mature IL-1α and calpain-1 were highly expressed in imquimod-induced psoriasis model and mouse IL-17a-neutralizing antibody treatment attenuated mS100a7a15 expression. At last, PD 151746 (calpain-1 inhibitor) treatment decreased epidermal thickness in imquimod-induced psoriasis model. Taken together, our results suggest that mature IL-1α induced by hS100A7 is via RAGE-p38 MAPK and calpain-1 pathway in keratinocyte and this mechanism may play an important role during psoriasis.

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“…1e and f, and Supplementary Fig. S2a), a protein that controls cell proliferation and differentiation, has AMP activity, and promotes the inflammatory process in psoriasis 37 . We also analyzed filaggrin expression but were unable to observe differences, probably because of the long half-life of the protein in the more differentiated skin layers ( Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

301 The psoriasis-associated IL-17A induces and cooperates with IL-36 cytokines to control keratinocyte differentiation and function

Pfaff

Kluwig

Marquardt

et al. 2017

Journal of Investigative Dermatology

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Psoriasis is a T H 17-driven inflammatory disease affecting a significant proportion of the world population. The molecular consequences of IL-17 signaling in the skin are only partially understood. Therefore, we evaluated the IL-17A effects on organotypic 3-dimensional skin models and observed that IL-17A interfered with keratinocyte differentiation. In agreement with this phenotype, IL-17A repressed the expression of many genes encoding structural proteins. Moreover, genes encoding anti-microbial peptides were induced, resulting in a strengthening of the chemical barrier. Finally, we observed enhanced expression of the three IL-36 cytokines IL-36α, β and γ. We found that IL-36γ was secreted from keratinocytes in an inactive form and that neutrophilic proteases, including elastase, were capable of activating this cytokine. Functionally and similar to IL-17A, truncated IL-36 cytokines interfered with keratinocyte differentiation in 3D models. The molecular analysis revealed strong cooperative effects of IL-17A and IL-36 cytokines in regulating target genes, which was dependent on the proteolytic activation of the latter. Together these findings suggest an amplification cycle that can be initiated by IL-17A, involving IL-36 cytokines and immune cell derived proteases and resulting in active IL-36 cytokines which synergize with IL-17A. This amplification cycle might be relevant for a persistent psoriatic phenotype.Psoriasis, a chronic autoimmune disease of the skin, affects approximately 2% of the population. Psoriasis is associated with systemic inflammatory processes including inflammatory arthritis, inflammatory bowel disease, and metabolic syndrome 1,2 . A typical manifestation of the disease is the hyperproliferation of keratinocytes with premature differentiation. This results in incomplete cornification with retention of nuclei in the stratum corneum, referred to as parakeratosis. Functionally this correlates with increased infiltrations of immune cells due to dendritic cells, macrophages, neutrophils and different subpopulations of T cells. These cells modify the cytokine milieu and thus affect the behavior of keratinocytes resulting in altered differentiation [1][2][3]

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S100A7: A rAMPing up AMP molecule in psoriasis

Cited by 41 publications

References 101 publications

Mechanical stress induced S100A7 expression in human dental pulp cells to augment osteoclast differentiation

Mechanical stress induced S100A7 expression in human dental pulp cells to augment osteoclast differentiation

Human S100A7 Induces Mature Interleukin1α Expression by RAGE-p38 MAPK-Calpain1 Pathway in Psoriasis

301 The psoriasis-associated IL-17A induces and cooperates with IL-36 cytokines to control keratinocyte differentiation and function

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