Autoradiographic Detection of Substance P Receptors in Normal and Psoriatic Skin

Pincelli, Carlo; Fantini, Fabrizio; Giardino, Luciana; Zanni, Massimo; Calzà, Laura; Sevignani, Cinzia; Giannetti, Alberto

doi:10.1111/1523-1747.ep12365423

Cited by 29 publications

(12 citation statements)

References 27 publications

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“…[18][19][20] Furthermore, human keratinocytes possess specific binding sites for and are activated by SP. 21,22 SP-containing nerve endings in the skin have been characterized by immunohistochemical analysis. 19,23 We have previously shown that the barrier function of the corneal epithelium is impaired in a rat model of neurotrophic keratopathy induced by thermocoagulation of the ophthalmic branch of the trigeminal nerve.…”

Section: Introductionmentioning

confidence: 99%

Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells

Murata

Nishida

2009

Cell Biochemistry & Function

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The formation of a barrier by tight junctions is important in epithelia of various tissues. Substance P (SP) and insulin-like growth factor (IGF)-1 synergistically promote barrier function in the corneal epithelium. We have now examined the effects of SP and IGF-1 on expression of the tight-junction protein zonula occludens (ZO)-1 in A431 human epidermoid carcinoma cells. Reverse transcription-polymerase chain reaction (RT-PCR) and immunoblot analyses revealed that SP and IGF-1 increased the amounts of ZO-1 mRNA and protein in these cells in a concentration-dependent manner, with neither SP nor IGF-1 alone having such an effect. The SP- and IGF-1-induced up-regulation of ZO-1 was accompanied by phosphorylation of extracellular signal-regulated kinase (ERK), and both of these effects were blocked by PD98059, an inhibitor of ERK activation. SP and IGF-1 also increased the transepithelial electrical resistance (TER) (an indicator of barrier function) of an A431 cell monolayer in a manner sensitive to PD98059. Our results thus suggest that the synergistic induction of ZO-1 expression by SP and IGF-1 may promote barrier function in skin epithelial cells.

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Section: Introductionmentioning

confidence: 99%

Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells

Murata

Nishida

2009

Cell Biochemistry & Function

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“…Environmental stimuli contribute to this process causing keratinocytes to initiate or to participate in the inflammatory reaction by their interaction with infiltrating mononuclear cells either by the release of proinflammatory cytokines or via the expression of intercellular adhesion molecules such as ICAM-1. Human keratinocytes have recently been reported to possess specific binding sites for SP and to be triggered by SP [8,9]. Thus, we sought to determine whether NK1 receptor agonists such as SP or Sar 9 Met(O 2 ) 11 SP (Sar Met) are involved in keratinocyte activation by evaluating ICAM-1 induction and cytokine production.…”

Section: Introductionmentioning

confidence: 99%

Substance P and keratinocyte activation markers: An in vitro approach

et al. 1996

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Substance P (SP) released by cutaneous C fibres is involved in the physiopathology of cutaneous lesions. As normal human keratinocytes have been reported to express SP receptors, we studied the effects of SP on keratinocyte activation markers such as ICAM-1 induction and cytokine production. Human keratinocytes derived from skin obtained during plastic surgery were cultured in defined medium (MCDB 153) and were stimulated by SP. Flow cytometry analysis showed that SP (10(-7) and 10(-5) M) as well as the specific NK1 agonist Sar9Met(O2)11SP (Sar Met) induced a slight but significant expression of ICAM-1 at the cell surface during treatment periods of 24 h and 48 h. SP (10(-5) M) also induced a significant but transient increase in the production of IL-1alpha, IL-1beta, IL-1 receptor antagonist and IL-8 which was detectable by ELISA techniques 6 h after stimulation. This elevation returned to constitutive levels 24 or 48 h postinduction. TNFalpha secretion was detected in stimulated cells only after 48 h. These results suggest that SP can activate keratinocytes and support its role in the local inflammatory reaction.

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“…The absence of SPB staining on basal keratinocytes may reflect either the absence or the occupation of the receptors by SP. Using autoradiography, no difference in the number or affinity of SPR per unit area was observed between normal and psoriatic skin [19] but binding in situ showed that SPR distribution was modified when compared to normal skin. The distribution of SPR on dermal structures was similar to normal skin.…”

Section: Discussionmentioning

confidence: 84%

“…The presence of SPR was already demonstrated on cultured keratinocytes by autoradiography [19] and binding assays [14] but has never been studied in cultured differentiated keratinocytes. In epidermal cultures, we showed that NK-1 receptors were unvaryingly expressed on superficial epidermal cells, except basal keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Expression of Substance P Receptors in Normal and Psoriatic Skin

et al. 1999

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Recently, sustance P receptors (SPR) have been detected in neonatal foreskin. Our purpose was to determine the expression of SPR in other localizations than neonatal foreskin. As SP has been implicated in the pathogenesis of inflammatory cutaneous lesions, we wondered whether SPR localization was modified in psoriatic lesions. In normal skin, SP binding sites were detected using biotinylated SP and abrogated by a specific NK1 antagonist (spantide) on blood vessels, sweat glands and hair follicles. In the normal epidermis, SPR were usually observed on granular layers but may also be observed on other cell layers. The SP binding processed on cultured keratinocytes demonstrated that SPR were expressed in the epidermis, except basal cell layers, confirming that keratinocytes constitutively express SPR. In skin lesions of psoriatic patients, SP binding sites were expressed on the uppermost keratinocytes which are not granular cells, and seem to be overexpressed. Our results raise the question of the role of SPR on psoriatic keratinocytes.

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Autoradiographic Detection of Substance P Receptors in Normal and Psoriatic Skin

Cited by 29 publications

References 27 publications

Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells

Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells

Substance P and keratinocyte activation markers: An in vitro approach

Expression of Substance P Receptors in Normal and Psoriatic Skin

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