Evidence map›Paper›PMID 34224892›Full record

ArticleActa biomaterialia2021

Genipin guides and sustains the polarization of macrophages to the pro-regenerative M2 subtype via activation of the pSTAT6-PPAR-gamma pathway.

Ilaha Isali, Phillip McClellan, Eswar Shankar, Sanjay Gupta, Mukesh Jain, James M Anderson, Adonis Hijaz, Ozan Akkus

Open access · greenAbstract read
In one paragraph

Article in Acta biomaterialia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. The Mechanistic Role of PPARPPAR research · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Tissue engineering. Part A · 2022
    Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Ilaha IsaliDepartment of Urology, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA.
Phillip McClellanDepartment of Mechanical and Aerospace Engineering, Case Western Reserve University, Cleveland, OH 44106, USA.
Eswar ShankarDepartment of Urology, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA.
Sanjay GuptaDepartment of Urology, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA.
Mukesh JainHarrington Discovery Institute and the Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, and the Case Cardiovascular Research Institute, Case Western Reserve University, USA.
James M AndersonDepartment of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Macromolecular Science, Case Western Reserve University, Cleveland, OH 44106, USA.
Adonis HijazDepartment of Urology, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA.
Ozan AkkusDepartment of Mechanical and Aerospace Engineering, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Orthopedics, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: oxa@case.edu.
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Amar Desai · 1987 to 2026
$142.3M
TRAINING PROGRAM IN MUSCULOSKELETAL RESEARCHT32AR007505 · NIAMS · CASE WESTERN RESERVE UNIVERSITY · PI TRIOLO, RONALD J · 1986 to 2023
$6.3M
Immunoregenerative treatment of Stress Urinary Incontinence by Autologous Macrophage TherapyR21HD095439 · NICHD · CASE WESTERN RESERVE UNIVERSITY · PI AKKUS, OZAN, HIJAZ, ADONIS K · 2018 to 2019
$440k
NCI NIH HHS P30 CA043703NIAMS NIH HHS T32 AR007505NICHD NIH HHS R21 HD095439
6 · The paper itself

Abstract

M2 macrophages are associated with deposition of interstitial collagen and other extracellular matrix proteins during the course wound healing and also inflammatory response to biomaterials. Developing advanced biomaterials to promote the M2 subtype may be an effective way to improve tissue reinforcement surgery outcomes. In this study, the effect of genipin, a naturally derived crosslinking agent, on M0 → M2-polarization was investigated. Genipin was introduced either indirectly by seeding cells on aligned collagen biotextiles that are crosslinked by the agent or in soluble form by direct addition to the culture medium. Cellular elongation effects on macrophage polarization induced by the collagen biotextile were also investigated as a potential inducer of macrophage polarization. M0 and M2 macrophages demonstrated significant elongation on the surface of aligned collagen threads, while cells of the M1 subtype-maintained a round phenotype. M0 → M2 polarization, as reflected by arginase and Ym-1 production, was observed on collagen threads only when the threads were crosslinked by genipin, implicating genipin as a more potent inducer of the regenerative phenotype compared to cytoskeletal elongation. The addition of genipin to the culture medium directly also drove the emergence of pro-regenerative phenotype as measured by the markers (arginase and Ym-1) and through the activation of the pSTAT6-PPAR-gamma pathway. This study indicates that genipin-crosslinked collagen biotextiles can be used as a delivery platform to promote regenerative response after biomaterial implantation. STATEMENT OF SIGNIFICANCE: The immune response is one of the key determinants of tissue repair and regeneration rate, and outcome. The M2 macrophage subtype is known to resolve the inflammatory response and support tissue repair by producing pro-regenerative factors. Therefore, a biomaterial that promotes M2 sub-type can be a viable strategy to enhance tissue regeneration. In this study, we investigated genipin-crosslinked electrochemically aligned collagen biotextiles for their capacity to induce pro-regenerative polarization of M0 macrophages. The results demonstrated that genipin, rather than matrix-induced cellular elongation, was responsible for M0 → M2 polarization in the absence of other bioinductive factors and maintaining the M2 polarized status of macrophages. Furthermore, we identified that genipin polarizes the M2 macrophage phenotype via activation of the pSTAT6-PPAR-gamma pathway.

Indexed as

MacrophagesPeroxisome Proliferator-Activated ReceptorsIridoidsMacrophage ActivationgenipinIridoidsPeroxisome Proliferator-Activated ReceptorsCollagenCytoskeleton structureGenipinMacrophage polarizationpSTAT6-PPAR-gamma pathway

Identifiers

PMID34224892
PMCPMC8373816
OpenAlexW3176608137

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.