Homodimerization of Interleukin-4 Receptor α Chain Can Induce Intracellular Signaling

Kammer, Winfried; Lischke, Antje; Moriggl, Richard; Groner, Bernd; Ziemiecki, Andrew; Gurniak, Christine B.; Berg, Leslie J.; Friedrich, Karlheinz

doi:10.1074/jbc.271.39.23634

Cited by 69 publications

(66 citation statements)

References 29 publications

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“…Cross-linking experiments with This can be explained by the presence of the IL-13R␣2 chain that we detect by RT-PCR and flow cytometry and which has been reported to bind IL-13 but not IL-4 with high affinity (43), thereby partially sequestering IL-13 in competition experiments. On the other hand, we cannot exclude the presence of IL-4R␣ homodimers in CCL202 fibroblasts in light of recent reports on chimeric receptors (44)(45)(46).…”

Section: Discussionmentioning

confidence: 73%

Interleukin (IL) 4 and IL-13 act on human lung fibroblasts. Implication in asthma.

Doucet¹,

Brouty‐Boyé²,

et al. 1998

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Section: Discussionmentioning

confidence: 73%

Interleukin (IL) 4 and IL-13 act on human lung fibroblasts. Implication in asthma.

Doucet¹,

Brouty‐Boyé²,

et al. 1998

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“…Mutational analyses of the cytoplasmic domain of IL-4Ra chain show that individual tyrosine residues are redundant for Stat3 activation. Signaling via homodimerization of IL-4Ra chain has been shown previously (23,47). However, a biological role for the IL-4Ra homodimers remains to be explored.…”

Section: Discussionmentioning

confidence: 99%

“…Human IL-4Ra cDNA was cloned into the expression vector pKCR in which the SV40 early gene promoter drove the transcription (17,23). Human IL-13Ra2 cDNA was cloned into pSecTagC (Invitrogen; ref.…”

Section: Methodsmentioning

confidence: 99%

Aberrant Stat3 Signaling by Interleukin-4 in Malignant Glioma Cells: Involvement of IL-13Rα2

Rahaman¹,

Vogelbaum²,

Haque

2005

Cancer Research

106

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Interleukin (IL)-4 exhibits antitumor activity in rodent experimental gliomas, which is likely mediated by the actions of IL-4 on a variety of immune cells present in and around the tumor masses. Here, we show that IL-4, which activates Stat6 in normal human astrocytes and in a variety of other cells, induces an aberrant activation of Stat3 in glioblastoma multiforme (GBM) cells but not in normal human astrocytes. Previously, we have shown that autocrine IL-6 signaling induces a persistent activation of Stat3. Now, we show that

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“…27 Finally, it was shown that homodimerization of the 140-kDa IL-4 receptor ␣-chain alone can induce intracellular signaling. 34,[52][53][54] Because Stat6 is involved in the induction of transcription of the IL-4 and IL-4 receptor ␣-chain genes, 55,56 our data point at the possible existence of an autocrine loop Immunohistochemical analysis of IL-4/IL-13 receptor ␣-chain (top panels) and PDGF-␤ receptor (bottom panels) demonstrates the induction of the expression of both receptor proteins in collared carotid arteries at 6 hours after injury (C and F, respectively). For both receptor molecules, very low or undetectable immunostaining is present in sham-operated uninjured arteries (B and E, respectively) and in negative control samples (A and D, respectively).…”

Section: Discussionmentioning

confidence: 99%

Upregulation and Activation of Stat6 Precede Vascular Smooth Muscle Cell Proliferation in Carotid Artery Injury Model

Baetta

Soma

De-Fraja

et al. 2000

ATVB

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Abstract-The role of signal transducers and activators of transcription (STAT) proteins in modulating proliferation and differentiation of various cell types in the hematopoietic system and the central nervous system has been well established. In contrast, the pathophysiological role of these proteins in vascular proliferative diseases has remained unproven, despite in vitro observations emphasizing the involvement of the STAT system in mediating vascular smooth muscle cell (VSMC) proliferation. On the basis of our previous observations demonstrating the occurrence of a specific modulation of Stat6 protein during the proliferative, migratory, and differentiation phases of the developing brain, we investigated whether Stat6 protein is present and modulated in arterial tissue challenged by perivascular injury. The time course of expression and localization of Stat6 after arterial injury was analyzed by immunohistochemistry, Western blot analysis, and confocal microscopy. Six hours after injury, the expression of Stat6 was markedly increased. This overexpression preceded the onset of VSMC proliferation and was downregulated starting from 7 days after injury, coincident with the decline of VSMC proliferation. Moreover, early after injury, Stat6 was predominantly localized at the nuclear level, denoting its functional activation. Conversely, Stat6 staining at later time points was largely cytosolic, suggesting silencing effects of this signaling pathway. These data indicate that Stat6 signaling may contribute to the modifications of gene expression underlying VSMC activation in the context of acute vascular proliferative diseases. [1][2][3][4][5][6] In normal arteries, VSMCs are in a fully differentiated, low proliferative rate phenotype; however, a number of growth factors or inflammatory cytokines elaborated by infiltrating leukocytes and activated intrinsic vascular cells can promote VSMCs to dedifferentiate and begin to replicate within the media, to migrate from the media into the intima, and to massively proliferate within the intima. 2,7,8 Changes in VSMC behavior induced by extracellular stimuli require the execution of a rapid and complex program of transcriptional events, which results in the emergence of VSMCs from quiescence (for a review see Reference 9). The nature of the molecular pathways specifically coupling the vascular injury stimuli to the VSMC dedifferentiation process is currently under intense investigation in an attempt to identify critical targets for interventional therapies. 10 -19 The quantitative and qualitative changes observed in VSMC gene expression during this transition involve, among others, the activation of distinct cytosolic signaling pathways. 9 A signaling cascade that has been correlated with mitogenic and pleiotropic functional responses induced by a variety of growth factors and cytokines involves the members of the Janus kinase (JAK) family of cytoplasmic tyrosine kinases (Jak1, Jak2, Jak3, and Tyk2) and the signal transducers and activators of transcription (STAT) pro...

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Homodimerization of Interleukin-4 Receptor α Chain Can Induce Intracellular Signaling

Cited by 69 publications

References 29 publications

Interleukin (IL) 4 and IL-13 act on human lung fibroblasts. Implication in asthma.

Interleukin (IL) 4 and IL-13 act on human lung fibroblasts. Implication in asthma.

Aberrant Stat3 Signaling by Interleukin-4 in Malignant Glioma Cells: Involvement of IL-13Rα2

Upregulation and Activation of Stat6 Precede Vascular Smooth Muscle Cell Proliferation in Carotid Artery Injury Model

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