JAK3/STAT6 Stimulates Bone Marrow–Derived Fibroblast Activation in Renal Fibrosis Article Swipe
Jingyin Yan
,
Zhengmao Zhang
,
Jun Yang
,
William E. Mitch
,
Yanlin Wang
·
YOU?
·
· 2015
· Open Access
·
· DOI: https://doi.org/10.1681/asn.2014070717
YOU?
·
· 2015
· Open Access
·
· DOI: https://doi.org/10.1681/asn.2014070717
Renal fibrosis is a final common manifestation of CKD resulting in progressive loss of kidney function. Bone marrow-derived fibroblast precursors contribute significantly to the pathogenesis of renal fibrosis. However, the signaling mechanisms underlying the activation of bone marrow-derived fibroblast precursors in the kidney are not fully understood. In this study, we investigated the role of the Janus kinase 3 (JAK3)/signal transducer and activator of transcription (STAT6) signaling pathway in the activation of bone marrow-derived fibroblasts. In cultured mouse monocytes, IL-4 or IL-13 activated STAT6 and induced expression of α-smooth muscle actin and extracellular matrix proteins (fibronectin and collagen I), which was abolished by a JAK3 inhibitor (CP690,550) in a dose-dependent manner or blocked in the absence of STAT6. In vivo, STAT6 was activated in interstitial cells of the obstructed kidney, an effect that was abolished by CP690,550. Mice treated with CP690,550 accumulated fewer bone marrow-derived fibroblasts in the obstructed kidneys compared with vehicle-treated mice. Treatment with CP690,550 also significantly reduced myofibroblast transformation, matrix protein expression, fibrosis development, and apoptosis in obstructed kidneys. Furthermore, STAT6-deficient mice accumulated fewer bone marrow-derived fibroblasts in the obstructed kidneys, produced less extracellular matrix protein, and developed much less fibrosis. Finally, wild-type mice engrafted with STAT6(-/-) bone marrow cells displayed fewer bone marrow-derived fibroblasts in the obstructed kidneys and showed less severe renal fibrosis compared with wild-type mice engrafted with STAT6(+/+) bone marrow cells. Our results demonstrate that JAK3/STAT6 has an important role in bone marrow-derived fibroblast activation, extracellular matrix production, and interstitial fibrosis development.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1681/asn.2014070717
- OA Status
- green
- Cited By
- 105
- References
- 49
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W1935205446
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W1935205446Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1681/asn.2014070717Digital Object Identifier
- Title
-
JAK3/STAT6 Stimulates Bone Marrow–Derived Fibroblast Activation in Renal FibrosisWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2015Year of publication
- Publication date
-
2015-06-02Full publication date if available
- Authors
-
Jingyin Yan, Zhengmao Zhang, Jun Yang, William E. Mitch, Yanlin WangList of authors in order
- Landing page
-
https://doi.org/10.1681/asn.2014070717Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
- OA URL
-
https://www.ncbi.nlm.nih.gov/pmc/articles/4657828Direct OA link when available
- Concepts
-
Bone marrow, Fibrosis, STAT6, Kidney, Cancer research, Fibroblast, Extracellular matrix, Medicine, Chemistry, Pathology, Endocrinology, Internal medicine, Biology, Cell biology, Interleukin 4, Cytokine, In vitro, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
105Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 10, 2024: 11, 2023: 9, 2022: 13, 2021: 14Per-year citation counts (last 5 years)
- References (count)
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49Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.fibroblast | 18, 38, 240 |
| abstract_inverted_index.mechanisms | 31 |
| abstract_inverted_index.monocytes, | 78 |
| abstract_inverted_index.obstructed | 128, 148, 170, 182, 210 |
| abstract_inverted_index.precursors | 19, 39 |
| abstract_inverted_index.transducer | 60 |
| abstract_inverted_index.underlying | 32 |
| abstract_inverted_index.(CP690,550) | 106 |
| abstract_inverted_index.accumulated | 141, 175 |
| abstract_inverted_index.activation, | 241 |
| abstract_inverted_index.demonstrate | 230 |
| abstract_inverted_index.expression, | 164 |
| abstract_inverted_index.fibroblasts | 145, 179, 207 |
| abstract_inverted_index.production, | 244 |
| abstract_inverted_index.progressive | 11 |
| abstract_inverted_index.understood. | 46 |
| abstract_inverted_index.(fibronectin | 95 |
| abstract_inverted_index.Furthermore, | 172 |
| abstract_inverted_index.development, | 166 |
| abstract_inverted_index.development. | 248 |
| abstract_inverted_index.fibroblasts. | 74 |
| abstract_inverted_index.interstitial | 124, 246 |
| abstract_inverted_index.investigated | 51 |
| abstract_inverted_index.pathogenesis | 24 |
| abstract_inverted_index.(JAK3)/signal | 59 |
| abstract_inverted_index.extracellular | 92, 186, 242 |
| abstract_inverted_index.manifestation | 6 |
| abstract_inverted_index.myofibroblast | 160 |
| abstract_inverted_index.significantly | 21, 158 |
| abstract_inverted_index.transcription | 64 |
| abstract_inverted_index.dose-dependent | 109 |
| abstract_inverted_index.marrow-derived | 17, 37, 73, 144, 178, 206, 239 |
| abstract_inverted_index.STAT6-deficient | 173 |
| abstract_inverted_index.transformation, | 161 |
| abstract_inverted_index.vehicle-treated | 152 |
| cited_by_percentile_year.max | 100 |
| cited_by_percentile_year.min | 96 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 5 |
| citation_normalized_percentile.value | 0.96111975 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |