Monocyte chemoattractant protein-1 (MCP-1/CCL2) in diabetic retinopathy: latest evidence and clinical considerations

Taghavi, Yousof; Hassanshahi, Gholamhossein; Kounis, Nicholas G.; Koniari, Ioanna; Khorramdelazad, Hossein

doi:10.1007/s12079-018-00500-8

Cited by 75 publications

(47 citation statements)

References 110 publications

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“…MCP-1 can chemotactically aggregate monocytes, which leads to capillary obstruction, vascular leakage and absence of perfusion. Increased expression of MCP-1 is also implicated in the pathogenesis of DR [27]. Here, we confirmed that LTF suppressed the expression of TNF-α, IL-1β, and MCP-1, which may contribute to the beneficial effects of LTF treatment.…”

Section: Discussionsupporting

confidence: 80%

Luo Tong formula attenuates retinal inflammation in diabetic rats via inhibition of the p38MAPK/NF-κB pathway

Pang

Song

et al. 2020

Chin Med

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Background: Diabetic retinopathy (DR) is a serious microvascular complication of diabetes and remains the leading cause of blindness in adults. Retinal inflammation is playing a crucial role in the development of DR, and targeting inflammatory mediators is a promising strategy for controlling DR. Here, we investigated compound Chinese medicine Luo Tong formula (LTF) alleviated retinal inflammatory responses in a STZ-induced diabetic rat model. Methods: Sprague-Dawley rats were divided into four groups: control, streptozotocin-induced diabetic, LTF-treated diabetic, and calcium dobesilate (CaD)-treated diabetic rats. Blood samples were collected for blood glucose examination. Hematoxylin-eosin and periodic acid-Schiff staining were conducted for light microscopy observations. Retinal cell apoptosis was detected using the TUNEL assay. Proteins expression was quantified by Western blotting and/or immunohistochemistry, and gene expression was assessed by real-time PCR. Results: Diabetic rats showed significant increases in the expression of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), nuclear factor-κB (NF-κB), and the phospho-p38 mitogen-activated protein kinase (p-p38-MAPK)/p38 MAPK ratio compared to control rats. LTF treatment significantly improved both retinal and pancreatic pathological injury, LTF treatment also inhibited inducible the p-p38 MAPK/p38 MAPK ratio and NF-κB activation and decreased the subsequent induction of the retinal expression of proinflammatory mediators TNF-α, IL-1β, MCP-1 and ICAM-1 compared to diabetic rats. LTF also exhibited a protective effect on islet function. Conclusions: LTF before the onset of DR can alleviate retinal pathological injury, LTF may play an anti-inflammatory role by inhibiting p38-MAPK and then inhibiting NF-κB pathway. But further studies are needed to confirm this conclusion. Trial registration This is an animal experiment, trial registration is not necessary.

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Section: Discussionsupporting

confidence: 80%

Luo Tong formula attenuates retinal inflammation in diabetic rats via inhibition of the p38MAPK/NF-κB pathway

Pang

Song

et al. 2020

Chin Med

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“…MCP-1 expression has also been detected in eyes with diabetic retinopathy. 18 Likewise, it is known to be involved in the process of developing a fibrotic capsule. 19 Previous research showed that MCP-1 was elevated after cataract surgery for 30 to 90 days, 20 while Inoue et al 21 and Jakobsson et al 11 demonstrated a significant increase of MCP-1 for more than 6 months after cataract surgery in adults.…”

Section: Discussionmentioning

confidence: 99%

Expression Profiles of Inflammatory Cytokines in the Aqueous Humor of Children after Congenital Cataract Extraction

Zhao

Deng

et al. 2020

Trans. Vis. Sci. Tech.

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To investigate the change in cytokine microenvironment of the aqueous humor (AH) after surgery in children with congenital or developmental cataracts. Methods: AH samples were obtained from 59 eyes diagnosed with a congenital or developmental cataract. Thirty-three of these eyes were aphakic following previous cataract surgery and were scheduled for secondary intraocular lens (IOL) implantation. Additionally, AH samples from 26 eyes that had not undergone surgery were taken. AH samples were then analyzed for 16 different inflammatory immune mediators using multiplex bead immunoassays and enzyme-linked immunosorbent assay (ELISA). Results: The mean interval between secondary IOL implantation and original cataract surgery was 24.85 months (range, 9-60 months). Levels of IL-6, IP-10 (CXCL10), MCP-1 (CCL2), and IL-2 were significantly elevated in the AH of eyes after surgery compared to eyes that did not undergo surgery (P < 0.001, P = 0.047, P = 0.006, P = 0.012, respectively). There was significant correlation between the levels of TGF-β2 and intraocular pressure (IOP) in postsurgical and nonsurgical eyes (r = 0.532, P = 0.006; r = 0.57, P = 0.001). Postsurgical outcomes, such as iris adhesions, capsular fibrosis, and capsular contraction, were found not to be significantly associated with cytokine levels in the AH after surgery; however, IL-6 levels in capsular exposure eyes were significantly higher than those in cortical closure eyes (P = 0.023). Conclusions: To our knowledge, this is the first study to report significantly increased proinflammatory cytokine levels in the AH after congenital cataract extraction in children. Our study also suggests that this proinflammatory state may be maintained for a prolonged period of time. Overall, these results give us insight into the relationship between the inflammatory cytokine microenvironment of the aqueous humor and potential long-term complications following congenital cataract surgery. Translational Relevance: The inflammatory cytokine microenvironment of the aqueous humor might help explain potential long-term complications after surgery in patients with congenital or developmental cataracts.

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“…Monocyte chemoattractant protein-1 attracts and activates monocyte and macrophages (112,113) and stimulates fibrosis and angiogenesis (114). MCP-1 is produced by Müller cells, microglia cells, astrocytes, retinal neurons, ECs, and retinal pigment epithelial cells in patients with diabetes (115). The migration of monocyte into the retina is mediated by MCP-1 coupling to its receptor CCR2 (116).…”

Section: Chemokine: Mcp-1mentioning

confidence: 99%

Endothelial Dysfunction in Diabetic Retinopathy

et al. 2020

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Diabetic retinopathy (DR) is a diabetic complication which affects retinal function and results in severe loss of vision and relevant retinal diseases. Retinal vascular dysfunction caused by multifactors, such as advanced glycosylation end products and receptors, pro-inflammatory cytokines and chemokines, proliferator-activated receptor-γ disruption, growth factors, oxidative stress, and microRNA. These factors promote retinal endothelial dysfunction, which results in the development of DR. In this review, we summarize the contributors in the pathophysiology of DR for a better understanding of the molecular and cellular mechanism in the development of DR with a special emphasis on retinal endothelial dysfunction.

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Monocyte chemoattractant protein-1 (MCP-1/CCL2) in diabetic retinopathy: latest evidence and clinical considerations

Cited by 75 publications

References 110 publications

Luo Tong formula attenuates retinal inflammation in diabetic rats via inhibition of the p38MAPK/NF-κB pathway

Luo Tong formula attenuates retinal inflammation in diabetic rats via inhibition of the p38MAPK/NF-κB pathway

Expression Profiles of Inflammatory Cytokines in the Aqueous Humor of Children after Congenital Cataract Extraction

Endothelial Dysfunction in Diabetic Retinopathy

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