Myeloid HO-1 modulates macrophage polarization and protects against ischemia-reperfusion injury

Zhang, Min; Nakamura, Kojiro; Kageyama, Shoichi; Lawal, Akeem O.; Gong, KeWei; Bhetraratana, May; Fujii, Takehiro; Sulaiman, Dawoud; Hirao, Hirofumi; Bolisetty, Subhashini; Kupiec‐Weglinski, Jerzy W.; Araujo, Jesús A.

doi:10.1172/jci.insight.120596

Cited by 93 publications

(85 citation statements)

References 35 publications

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“…In addition, heme oxygenase HO-1, the derivable isoform of the heme-degrading enzyme HO, plays an important role in inflammation and immunoregulation of homeostasis. Myeloid HO-1 expression modulates macrophage polarization to M2 [72,73]. Furthermore, high HO-1 level increased the expression of osteonectin, OPG and BMP-2, and increase osteoblast function and differentiation [74].…”

Section: Discussionmentioning

confidence: 99%

Icariin/Aspirin Composite Coating on TiO2 Nanotubes Surface Induce Immunomodulatory Effect of Macrophage and Improve Osteoblast Activity

You

Chen

et al. 2020

Coatings

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Surface coating modification of titanium-based alloys is an efficient way to accelerate early osseointegration in dental implant fields. Icariin (ICA) is a traditional Chinese medicine that has bone activating functions, while aspirin (ASP) is a classical non-steroidal anti-inflammatory drug with good antipyretic and analgesic capabilities. Moreover, poly(lactic–co–glycolic acid) (PLGA) has attracted great attention due to its excellent biocompatibility and biodegradability. We superimposed an ASP/PLGA coating onto ICA loaded TiO2 nanotubes structure so as to establish an icariin/aspirin composite coating on TiO2 nanotubes surface. Scanning electron microscopy, X-ray photoelectron spectroscopy, a contact angle test and a drug release test confirmed the successful preparation of the NT–ICA–ASP/PLGA substrate, with a sustained release pattern of both ICA and ASP. Compared to those cultured on the Ti surface, macrophage cells on the NT-ICA-ASP/PLGA substrate displayed decreased M1 proinflammatory and enhanced M2 proregenerative genes and proteins expression, which implied activated immunomodulatory effect. Moreover, when cultured with conditioned medium from macrophages, osteoblast cells on the NT-ICA-ASP/PLGA substrate revealed improved cell proliferation, adhesion and osteogenic genes and proteins expression, compared with those on the Ti surface. The abovementioned results suggest that the established NT-ICA-ASP/PLGA substrate is a promising candidate for functionalized coating material in Ti implant surface modification.

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Section: Discussionmentioning

confidence: 99%

Icariin/Aspirin Composite Coating on TiO2 Nanotubes Surface Induce Immunomodulatory Effect of Macrophage and Improve Osteoblast Activity

You

Chen

et al. 2020

Coatings

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“…This phenomenon demonstrated that some other pathway might contribute to CRYAB modulation in hepatic IRI. Based on that, our vision shifted onto the relevance between CRYAB and mTOR pathway regarding the critical role of M2 polarization in organ IRI 35,36 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miR-450b-5p ameliorates hepatic ischemia/reperfusion injury via targeting CRYAB

et al. 2020

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Hepatic ischemia/reperfusion injury (IRI) is an unavoidable course in liver transplantation, during which the immune response of inflammation plays a leading part. MicroRNA-450b-5p (miR-450b-5p), which has been reported to participate in several inflammatory diseases, was investigated in this study. The purpose of this study is to identify the potential function of miR-450b-5p toward remission of hepatic IRI and elucidate the specific mechanism. Herein we found that expression of miR-450b-5p, interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and IL-6 was stimulated in hepatic IRI. Inhibition of miR-450b-5p could remarkably alleviate mouse hepatic IRI and improve liver function measured by hematoxylin-eosin (HE) staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), and enzyme-linked immunosorbent assay (ELISA). We further assessed protein expression undergoing Western blot and immunofluorescence, and discovered that miR-450b-5p suppressed alpha B-crystallin (CRYAB), thus restraining the inhibitory κB kinase (IKK) β-mediated canonical nuclear factor-κB (NF-κB) signaling, instead of the noncanonical path guided by IKKα in hepatic IRI. In addition, we demonstrated CRYAB as an activator of M2 polarization through protein kinase B (Akt) 1/mammalian target of rapamycin (mTOR), thus resulting in relief of liver IRI. Combination treatment containing both paths revealed a better antidamage efficacy than adjusting either path alone, suggesting that the joint therapy might be a promising solution in hepatic IRI.

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“…Min et al used myeloid-specific HO-1 gene knockout (mHO-1-KO) and transgenic (mHO-1-Tg) mice to delete or overexpress HO-1, verifying that myeloid HO-1 expression improves liver IR damage by promoting macrophage M2 phenotypic polarization. Interestingly, in human liver transplantation biopsies, subjects with higher HO-1 levels showed a lower expression of M1 markers and higher expression of M2 markers as well as reduced hepatic damage and an improved prognosis (24). Soluble fibrinogen-like protein 2 (sFGL2) promotes the secretion of anti-inflammatory cytokines (IL-10, TGF-β) and the high expression of CD206 and inhibits the activity of STAT1 and NF-κB signaling pathways.…”

Section: Polarization Of Kcs In I/rmentioning

confidence: 99%

Effect of Hepatic Macrophage Polarization and Apoptosis on Liver Ischemia and Reperfusion Injury During Liver Transplantation

Mao

et al. 2020

Front. Immunol.

111

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Ischemia-reperfusion (I/R) injury is injury caused by a limited blood supply and subsequent blood supply recovery during liver transplantation. Serious ischemia-reperfusion injury is the main cause of transplant failure. Hepatic I/R is characterized by tissue hypoxia due to a limited blood supply and reperfusion inducing oxidative stress and an immune response. Studies have confirmed that Kupffer cells (KCs), resident macrophages in the liver, play a key role in aseptic inflammation induced by I/R. In liver macrophage polarization, M1 macrophages activated by interferon-γ (IFN-γ) and lipopolysaccharide (LPS) exert a pro-inflammatory effect and release a variety of inflammatory cytokines. M2 macrophages activated by IL-4 have an anti-inflammatory response. M1-type KCs are the dominant players in I/R as they secrete various pro-inflammatory cytokines that exacerbate the injury and recruit other types of immune cells via the circulation. In contrast, M2-type KCs can ameliorate I/R through unregulated anti-inflammatory factors. A new notion has been proposed that KC apoptosis may influence I/R in yet another manner as well. Management of KCs is expected to help improve I/R. This review summarizes the effects of hepatic macrophage polarization and apoptosis on liver I/R.

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Myeloid HO-1 modulates macrophage polarization and protects against ischemia-reperfusion injury

Cited by 93 publications

References 35 publications

Icariin/Aspirin Composite Coating on TiO2 Nanotubes Surface Induce Immunomodulatory Effect of Macrophage and Improve Osteoblast Activity

Icariin/Aspirin Composite Coating on TiO2 Nanotubes Surface Induce Immunomodulatory Effect of Macrophage and Improve Osteoblast Activity

Inhibition of miR-450b-5p ameliorates hepatic ischemia/reperfusion injury via targeting CRYAB

Effect of Hepatic Macrophage Polarization and Apoptosis on Liver Ischemia and Reperfusion Injury During Liver Transplantation

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