Increase of glandular epithelial cell clusters by an external volume expansion device promotes adipose tissue regeneration by recruiting macrophages

Abstract

Background: There is a clinical need for the use of engineered adipose tissue in place of surgical reconstruction. We previously found that the external volume expansion (EVE) device increased special cell clusters in well-vascularized connective stroma during adipose regeneration. However, the origin of these cell clusters and their role in adipose tissue regeneration remain unknown. Aim: In the present study, we evaluated EVE in the construction of expanded prefabricated adipose tissue (EPAT) in a rat model. Methods: Rats were randomized into an EVE suction group and a control group, with 24 rats in each group. The structure and origin of the special cell clusters were determined by hematoxylin and eosin staining, and immunohistochemistry; their role in adipose tissue regeneration was investigated by immunohistochemistry and Western blot analyses. Results: Special cell clusters began to increase at week 1 with a peak at week 4, and then receded from weeks 8 to 12. Clusters were identified as glandular epithelial cells as determined by their gland-like structure and expression of specific markers. The cell clusters induced significant infiltration of macrophage antigen-2 (Mac-2) positive macrophages by secreting monocyte chemoattractant protein-1 (MCP-1) at the early stage of suction. Subsequently, these infiltrated macrophages expressed massive vascular endothelial growth factor (VEGF) to promoted angiogenesis. Conclusion: EVE generated glandular epithelial cell clusters, which recruited macrophages to promote angiogenesis and subsequent adipose tissue regeneration. These findings shed light on the mechanisms underlying the effects of EVE devices on adipose tissue regeneration.

Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages

“…The mRNA levels of the total macrophage marker Mac-2 [ 4 , 5 ] in wild-type mice and PD-1 −/− mice were significantly higher than those in the noninjured group at 1, 3, 7, and 14 days after injury ( P < 0 05). However, there was no significant difference between the PD-1 −/− and wild-type mice ( P > 0.05) (Fig.…”

“…We studied this issue. In the present study, Mac-2 was used as a marker of total macrophages [ 4 , 5 ], iNOS and CD86 were used as pro-inflammatory macrophage markers [ 14 , 15 ], and Arg1, CD206, and CD163 were used as anti-inflammatory macrophage markers [ 14 , 15 ]. The present study found that the number of total macrophages, pro-inflammatory macrophages, and anti-inflammatory macrophages increased in the early stage (1–3 days) of skeletal muscle injury in wild-type mice.…”

“…Macrophages infiltrate into the injured site after skeletal muscle injury and play an important role in repairing injured skeletal muscle. It can specifically express macrophage antigen-2 (Mac-2) [ 4 , 5 ]. There are two basic types of macrophages, pro-inflammatory and anti-inflammatory macrophages [ 6 , 7 ].…”

Rutaecarpin reduces lipids by DGKθ‐dependent activation of PPARα

“…Proteins were extracted from cultured cells or tissues, and Western blot analyses of the extracted proteins were performed with the enhanced chemiluminescence (ECL) system (Thermo Fisher Scientific) [7, 21]. Blots were probed with anti‐DGKθ (Proteintech Group), anti‐APOC3 and anti‐PPARα (Wanlebio), anti‐HNF1B (HUABIO), anti‐glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH; Engibody Biotechnology, Inc.), and goat anti‐mouse immunoglobin G (IgG) and goat anti‐rabbit IgG (horseradish peroxidase, ZSGB‐BIO).…”

The Application and Mechanism of Action of External Volume Expansion in Soft Tissue Regeneration

“…EVE was shown to generate specific cell clusters. 100 These clusters contained glandular epithelial-like cells, as evidenced by their gland-like structure and expression of specific markers. Soon after their generation, these cell clusters began to secrete monocyte chemoattractant protein-1 (MCP-1), which induced infiltration of significant numbers of macrophages.…”