Maxed out macs: physiologic cell clearance as a function of macrophage phagocytic capacity

Zent, Clive S.; Elliott, Michael R.

doi:10.1111/febs.13961

Cited by 67 publications

(69 citation statements)

References 144 publications

(217 reference statements)

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“…In contrast, intraepithelial macrophages located in prostatic lesions were mostly enlarged, rounded cells, containing numerous, and large autophagic vacuoles. It has been shown that engulfment of multiple targets induces molecular and morphological changes in macrophages, making them rounder in shape with less membrane extension, thus reducing their capacity to engulf new targets 48 . Such macrophage features corroborate our present findings.…”

Section: Discussionsupporting

confidence: 91%

“…Such macrophage features corroborate our present findings. One possible mechanism for enhancing the degradation of excess cytoplasmic cargo by macrophages is the involvement of autophagic pathways, which would lead to the LC3‐associated phagocytosis 48 . Consistent with these events, the engorged macrophages were usually found in clusters within the prostate lesions and were proven positive for the autophagic‐specific marker LC3.…”

Section: Discussionmentioning

confidence: 85%

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Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

et al. 2020

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Background Prostate cancer remains one of the most common cancers in men. Macrophages are thought to be important regulators in cancers, and their potential involvement in prostate cancer should not be overlooked. Therefore, the association between macrophages and the pre‐tumorous changes in prostate epithelium during aging deserves further investigation. Objectives We sought to investigate whether macrophages would be recruited into the prostate epithelium that display pathological lesions commonly found during aging. Materials and methods Prostates of aging rats, with and without treatment with a combination of testosterone and estradiol, were examined for premalignant and malignant epithelial lesions. For comparison, prostates of castrated rats were also investigated. Results Intraepithelial macrophages were found restricted to areas of premalignant and malignant lesions. An unprecedented interaction between macrophages and basal cells was observed in the aging pathological lesions. The intraepithelial macrophages were associated with autophagy, in contrast to those found after castration. In prostate lesions, the intraepithelial macrophages had TAM phenotype (CD68+/iNOS+/CD206+/ARG+), denoting a possible involvement in cancer progression. However, M2 macrophages (CD68+/CD163+) were recruited into the epithelium after castration, possibly to phagocytize cells undergoing apoptosis. Discussion and conclusion In conclusion, macrophages were recruited into the prostate epithelium and presented diverse phenotypes and morphology, consistent with changes reflected in the hormonal environment. Macrophages with the TAM phenotype were found restricted to areas of premalignant and malignant lesions in aging prostates, denoting a possible involvement in cancer progression. In contrast, M2 macrophages were found in the regressed epithelium after castration.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 85%

Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

et al. 2020

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“…Phagocytosis of dying or dead cells by phagocytes such as macrophages is known as efferocytosis (Birge et al, 2016; Zent and Elliott, 2017). Removal of dead or dying cells by efferocytosis is critical for maintaining homeostasis and preventing inflammation and autoimmune reactions (Elliott and Ravichandran, 2016).…”

Section: Introductionmentioning

confidence: 99%

Protein S and Gas6 induce efferocytosis of HIV-1-infected cells

et al. 2018

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Efferocytosis, the phagocytic clearance of apoptotic cells, can provide host protection against certain types of viruses by mediating phagocytic clearance of infected cells undergoing apoptosis. It is known that HIV-1 induces apoptosis and HIV-1-infected cells are efferocytosed by macrophages, although its molecular mechanisms are unknown. To elucidate the roles that efferocytosis of HIV-1-infected cells play in clearance of infected cells, we sought to identify molecules that mediate these processes. We found that protein S, present in human serum, and its homologue, Gas6, can mediate phagocytosis of HIV-1-infected cells by bridging receptor tyrosine kinase Mer, expressed on macrophages, to phosphatidylserine exposed on infected cells. Efferocytosis of live infected cells was less efficient than dead infected cells; however, a significant fraction of live infected cells were phagocytosed over 12 h. Our results suggest that efferocytosis not only removes dead cells, but may also contribute to macrophage removal of live virus producing cells.

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“…The CD45 transmembrane protein is a principal component of the negative feedback signal in both efferocytosis and ADCP. CD45 functions as a "do not eat me" signal when it couples with SIRPα receptors on macrophages [61]. Expulsed cancer cell nuclei no longer express CD45; therefore, there is no negative feedback signals for macrophage engulfment.…”

Section: Nuclear Expulsion and The Formation Of Cancer Fusion Cells (mentioning

confidence: 99%

The natural adaptive evolution of cancer: The metastatic ability of cancer cells

Olteanu¹,

Mihai

Bojin³

et al. 2020

Bosn J of Basic Med Sci

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The ability of cancer to adapt renders it one of the most challenging pathologies of all time. It is the most dreaded pathological entity because of its capacity to metastasize to distant sites in the body, and 90% of all cancer-related deaths recorded to date are attributed to metastasis. Currently, three main theories have been proposed to explain the metastatic pathway of cancer: the epithelial–mesenchymal transition (EMT) and mesenchymal–epithelial transition (MET) hypothesis (1), the cancer stem cell hypothesis (2), and the macrophage–cancer cell fusion hybrid hypothesis (3). We propose a new hypothesis, i.e., under the effect of particular biochemical and/or physical stressors, cancer cells can undergo nuclear expulsion with subsequent macrophage engulfment and fusion, with the formation of cancer fusion cells (CFCs). The existence of CFCs, if confirmed, would represent a novel metastatic pathway and a shift in the extant dogma of cancer; consequently, new treatment targets would be available for this adaptive pathology.

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Maxed out macs: physiologic cell clearance as a function of macrophage phagocytic capacity

Cited by 67 publications

References 144 publications

Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

Protein S and Gas6 induce efferocytosis of HIV-1-infected cells

The natural adaptive evolution of cancer: The metastatic ability of cancer cells

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