Objective To explore the role of activated macrophage in the repair of traumatic optic nerve injury in an animal model of incomplete traumatic optic nerve injury with lens damage.Methods One hundred and twelve healthy New Zealand big ear white rabbits were divided into two groups (experimental and control groups) randomly. According to the different time points (one, four, seven, ten, 14, 21 and 28 days), each group was further divided into seven subgroups, each subgroup had eight rabbits. Traumatic optic neuropathy and lens damage were induced in one eye of each rabbit by fluid percussion brain injury device (FPI); those eyes were the experimental group. The eyes of control group only had traumatic optic neuropathy. The functional and morphological changes of retina and optic nerve were evaluated by histopathology and flashvisual evoked potential (FVEP).Results FVEP P100 latency was (42.74plusmn; 5.83) ms, P100 amplitude was (7.98 plusmn; 2.15) mu;V before optic nerve injury was induced. One day after the injury, the P100latency increased and the P100amplitude reduced significantly. The P100 latency reached the longest at ten days after injury, and then recovered gradually. The P100 amplitude reached the lowest at seven days after injury, and then recovered gradually. The histopathological examination showed activated macrophages were not detected in the retina and optic nerve at day one after the injury, then they increased gradually and reached their peak (91.25plusmn;6.91) at day ten, and decreased after that, the difference was statistically significant (F=21.277, P=0.000); retinal ganglion cell axon regeneration began at day seven after the injury with an average of (6.38plusmn;1.85). The axons increased gradually and reached their peak (49.63plusmn;2.50) at day 28, and the changes were significant (F=7.711, P=0.000). Conclusions Incomplete optic nerve injury can recover gradually if there is lens damage at the same time. Activated macrophage may play an important role in this recovery process.
Objective To investigate the effect of peritoneal exudative cells as feeder cells on growth state of primary culture of adult rat retinal Muuml;ller cells. Methods Peritoneal exudative cells were gained from adult rats, which were identified with specifically biological marker of macrophage (CD68). The phagocytosis was evaluated by the ink particles experiment. Retinal Muuml;ller cells of adult rats were cultured by enzyme digestion method, and identified by GFAP and vimentin immunocytochemically. As the feeder cells, peritoneal exudative cells were cocultured with Muuml;ller cells. The proliferation cycle of Muuml;ller cells was assayed by flow cytometry. One-step TUNEL staining was employed to detect the apoptotic Muuml;ller cells. Results Over ninety-five percent of rat peritoneal exudative cells were macrophage, which have a favourable phagocytic ability for the ink particles. The primary cultured Muuml;ller cells adhered to the wall of flask and grew fast, with large applanate cell bodies. The third-generation cells grew slowly. After cocultured with feeder cells, the Muuml;ller cells showed more rapid growth rate with more cells in S and G2/M phase(S phase, t=4.172, Plt;0.001; G2/M phase, t=3.562, Plt;0.01） and less apoptotic rate (t=3.804, Plt;0.01). The growing cycle was cut down from 25-30 days to 1822 days for the firstgeneration cells, from 10-15 days to 7-10 days for the second-generation cells. Conclusion It is an effective method to use the peritoneal exudative cells as feeder cells cocultured with primary culture of retinal Muuml;ller cells, which can shorten the culture period of Muuml;ller cells in adult rats.
PURPOSE: To investigate the activation and immune respones of lymphocytes in epiretinal membranes (ERMs)and subretinaI membranes (SRMs). METHODS: A panel of morioclonal antibodies against CD23 (activated B cell), CD25 (activated T cell), CD68(macrophages) and HLA-DR (human leukocyte antigen II antigen)were used for the study of 20 specimens of ERMs from 20 patients with proliferative vitreoretinopathy (PVR),traumatic PVR and secondary traction retinal detachment,and 2 SRMs from PVR and traumatic PVR, with positive and negative reaction specimens as controls. RESULTS:Four cases of ERMs were found to be CD23 and CD25 positive respectively,and one case of SRMs to be CD23 and CD25 positive respectively. All the specimens of ERMs and SRMs revealed CD68 and HLA-DR positive in this series. CONCLUSIONS :There might be an aberrant immunoreaction mediated by T and B cells in the ERMs and the SRMs,and they might play an important role in the patbogenesis of PVR,traumatic PVR and secondary traction retinal detachments. （Chin J Ocul Fundus Dis,1996,12: 147-150）
ObjectiveTo investigate the expressions of microRNA-155 (miR-155) in different phenotypes of activated macrophages. MethodsThe THP-1 cells underwent polarized activation into M1, M2 or tumor-associated macrophages (TAMs), and the phenotypes were confirmed by flow cytometry. The miR-155 expression was determined by qRt-PCR in M1 macrophages, M2 macrophages and TAMs. ResultsThe miR-155 expression significantly decreased in the M2 macrophages (1.83±0.337, P=0.000), TAMs (1.60±0.233, P=0.000) compared with the M1 (6.580±0.637). The phenotype of TAMs was similar to M2. There was no statistically significant difference between TAMs and M2 macrophages in the expression of miR-155 (P=0.546). ConclusionDifferent expressions of miR-155 in macrophages M1-type and M2-type may be associated with the differentiation or their cellular functions. The phenotypic characteristics TAMs may transform to macrophages to M2-type. And they may have the same functions.
Macrophages are major effecter cells of nonspecific immune response, the polarization of which plays a great role in inflammation, repairing and angiogenesis. According to functional phenotypes, macrophages can be polarized to classically activated type (M1), which could promote angiogenesis, and alternatively activated type (M2), which could inhibit angiogenesis. The proportion of M1/M2 could modulate the growth of choroidal neovascularization (CNV). Under the conditions of aging and injury within the retina, macrophages may polarize to M2, which could generate several proangiogenic factors, initiating and promoting the formation of angiogenesis and fibrous scar. Therefore, regulation of macrophage polarization is expected to inhibit angiogenesis and provide new insight for treatment of CNV.
Retinal macrophages and (or) microglial cells play important roles in regulating inflammation, angiogenesis and tissue repairing, thus affect the development and prognosis of ischemic retinal disease, ocular immune diseases and ocular tumors. Reversing the polarization imbalance of these cells may provide new therapeutic strategies for ischemic retinal disease and ocular immune diseases. The duality of the polarization direction of these cells is still controversial in the inflammatory reaction and pathological angiogenesis of ischemic retinal disease. Meanwhile, the plasticity and diversity of the function need to be further studied and discussed.
Objective To summary the regulatory effect of mechanical stimulation on macrophage polarization in wound healing, and explore the application prospect of mechanical stimulation in tissue engineering. Methods The related domestic and foreign literature in recent years was extensive reviewed, and the different phenotypes of macrophages and their roles in wound healing, the effect of mechanical stimulation on macrophage polarization and its application in tissue engineering were analyzed. Results Macrophages have functional diversity, with two phenotypes: pro-inflammatory (M1 type) and anti-inflammatory (M2 type), and the cells exhibit different activation phenotypes and play corresponding functions under different stimuli. The mechanical force of different types, sizes, and amplitudes can directly or indirectly guide macrophages to transform into different phenotypes, and then affect tissue repair. This feature can be used in tissue engineering to selectively regulate macrophage polarization. Conclusion Mechanical stimulation plays an vital role in regulating macrophage polarization, but its specific role and mechanism remain ambiguous and need to be further explored.
Macrophages are important immune effector cells with significant plasticity and heterogeneity in the body immune system, and play an important role in normal physiological conditions and in the process of inflammation. It has been found that macrophage polarization involves a variety of cytokines and is a key link in immune regulation. Targeting macrophages by nanoparticles has a certain impact on the occurrence and development of a variety of diseases. Due to its characteristics, iron oxide nanoparticles have been used as the medium and carrier for cancer diagnosis and treatment, making full use of the special microenvironment of tumors to actively or passively aggregate drugs in tumor tissues, which has a good application prospect. However, the specific regulatory mechanism of reprogramming macrophages using iron oxide nanoparticles remains to be further explored. In this paper, the classification, polarization effect and metabolic mechanism of macrophages were firstly described. Secondly, the application of iron oxide nanoparticles and the induction of macrophage reprogramming were reviewed. Finally, the research prospect and difficulties and challenges of iron oxide nanoparticles were discussed to provide basic data and theoretical support for further research on the mechanism of the polarization effect of nanoparticles on macrophages.