Molecular cloning and biophysical characterization of CXCL3 chemokine

Gulati, Khushboo; Gangele, Krishnakant; Agarwal, Nipanshu; Jamsandekar, Minal; Kumar, Deepak; Poluri, Krishna Mohan

doi:10.1016/j.ijbiomac.2017.09.032

Cited by 20 publications

(20 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CXCL3 is another member of CINCs, and it is the least researched chemokine in the context of nociception processes. Despite the fact that structural details and receptor binding interactions in the case of CXCL1 and CXCL2 have been elucidated for years, the information regarding the structural and biophysical characteristics of CXCL3 became available as late as 2018, when Gulati et al (30) successfully cloned, expressed, and purified the recombinant CXCL3. The authors revealed that although the overall structural and oligomerization features of CXCL3 and CXCL1/2 are similar, prominent differences can be observed on their characteristic surface structures, thus indicating a functional divergence.…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of these pathways in the development of neuropathy has been known for many years, also in our model (11, 39, 40). CXCL3 is strongly expressed in a number of tumorous conditions (30, 92); however, its role in the context of neuropathy has yet to be studied. Our results regarding time course changes of mRNA and protein indicate that of all CINCs, CXCL3 is the most important in the development of neuropathic pain, and its protein level undergoes upregulation up to 7 days.…”

Section: Discussionmentioning

confidence: 99%

“…Among CINCs, three types have been distinguished and are referred to as CINC-1 (chemokine CXC ligand 1, CXCL1; growth-regulated GRO protein alpha, GROα; melanoma growth stimulating activity alpha, MSGA-α; keratinocyte-derived chemokines, KC), CINC-2 (chemokine CXC ligand 3, CXCL3; growth-regulated GRO protein gamma, GROγ; macrophage inflammatory protein-2-beta, MIP2β), and CINC-3 (chemokine CXC ligand 2, CXCL2; growth-regulated protein beta, GROβ; macrophage inflammatory protein 2-alpha, MIP2α). In 2018, Gulati et al (30) showed that the CINC family arose as a result of two rounds of gene duplication in the course of evolution. The family members are closely related to each other, and biological studies reported their differential tissue expression and regulation.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury

et al. 2019

View full text Add to dashboard Cite

Recently, the role of CXCR2 in nociception has been noted. Our studies provide new evidence that the intrathecal administration of its CINC ligands (Cytokine-Induced Neutrophil Chemoattractant; CXCL1-3) induces pain-like behavior in naïve mice, and the effect occurring shortly after administration is associated with the neural location of CXCR2, as confirmed by immunofluorescence. RT-qPCR analysis showed, for the first time, raised levels of spinal CXCR2 after chronic constriction injury (CCI) of the sciatic nerve in rats. Originally, on day 2, we detected escalated levels of the spinal mRNA of all CINCs associated with enhancement of the protein level of CXCL3 lasting until day 7. Intrathecal administration of CXCL3 neutralizing antibody diminished neuropathic pain on day 7 after CCI. Interestingly, CXCL3 is produced in lipopolysaccharide-stimulated microglial, but not astroglial, primary cell cultures. We present the first evidence that chronic intrathecal administrations of the selective CXCR2 antagonist, NVP CXCR2 20, attenuate neuropathic pain symptoms and CXCL3 expression after CCI. Moreover, in naïve mice, this antagonist prevented CXCL3-induced hypersensitivity. However, NVP CXCR2 20 did not diminish glial activation, thus not enhancing morphine/buprenorphine analgesia. These results provide novel insight into the crucial role of CXCR2 in neuropathy based on CXCL3 modulation, which may become a potential therapeutic target in pain treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Importantly, we presented the oncogenic role of circMET (also known as hsa_circ_0082003 in circBase), which was significantly upregulated in NSCLC tissues and is closely associated with the poor prognosis of NSCLC patients. Furthermore, we identified that circMET could promote the progression of NSCLC cells by sponging oncogenic miR-145-5p [ 18 , 19 ] to upregulate chemokine (C-X-C motif) ligand 3 (CXCL3) [ 20 , 21 ] expression. Therefore, circMET may serve as a novel diagnostic biomarker and promising therapeutic target for NSCLC patients.…”

Section: Introductionmentioning

confidence: 99%

circMET promotes NSCLC cell proliferation, metastasis, and immune evasion by regulating the miR-145-5p/CXCL3 axis

Pei

Chen

Long

et al. 2020

Aging

View full text Add to dashboard Cite

In recent years, circular RNAs (circRNAs) have been increasingly reported to play a crucial role in the proliferation, migration, and invasion of non-small-cell lung cancer (NSCLC) cells. However, the circRNA MET (circMET) oncogenic mechanism that drives NSCLC development and progression remains largely unknown. In this study, the present results demonstrated that circMET expression was significantly higher in NSCLC tissues than in peritumoral tissues using quantitative real-time polymerase chain reaction. Notably, NSCLC patients with a large tumor diameter, poor differentiation and lymphatic metastasis had high RNA levels of circMET. Moreover, high circMET expression served as an independent risk factor for short overall survival (OS) and progression-free survival (PFS) in NSCLC patients. Next, we validated that circMET overexpression can enhance NSCLC cell proliferation, metastasis, and immune evasion in vitro. Mechanistically, our study uncovers that circMET acts as a miR-145-5p sponge to upregulate CXCL3 expression. Collectively, circMET regulates the miR-145-5p/CXCL3 axis and serves as a novel, promising diagnostic and prognostic biomarker in patients with NSCLC.

show abstract

“…Ifitm 1 and 2, which were upregulated 5 and 3-fold respectively, have emerged as potent viral inhibitors of a broad range of RNA viruses, although they have been found to be overexpressed in colitis-associated colon cancer and in severely inflamed mucosa of UC and CD patients (44). Cxcl3, which was upregulated 29-fold, plays a role in inflammation and as a chemoattractant for neutrophils that are important in controlling fungal organisms (45). Csf3r, which was upregulated 4.4-fold, has been shown to play a crucial role in the proliferation, differentiation and survival of cells along the neutrophilic lineage (46).…”

Section: Resultsmentioning

confidence: 99%

Setting off the Alarms:Candida albicansElicits Pro-Inflammatory Differential Gene Expression in Intestinal Peyer’s Patches

Singh

Song

et al. 2019

Preprint

View full text Add to dashboard Cite

24Candida albicans has been associated with a number of human diseases that pertain to 25 the gastrointestinal (GI) tract. However, the details of how gut-associated lymphoid tissues 26 (GALT) such as Peyer's patches (PPs) in the small intestine play a role in immune surveillance 27 and microbial differentiation, and what mechanisms PP use to protect the mucosal barrier in 28 response to fungal organisms such as C. albicans, are still unclear. We particularly focus on PPs 29 as they are the immune sensors and inductive sites of the gut that influence inflammation and 30 tolerance. We have previously demonstrated that CD11c + phagocytes located in the sub-31 epithelial dome (SED) within PPs sample C. albicans. To gain insight on how specific cells 32within PPs sense and respond to the sampling of fungi, we gavaged mice with C. albicans strains 33 ATCC 18804 and SC5314 as well as Saccharomyces cerevisiae. We measured the differential 34 gene expression of sorted CD45 + B220 + B-cells, CD3 + T-cells, and CD11c + DCs within the first 35 24 hrs post-gavage using nanostring nCounter® technology. The results reveal that at 24 hrs, PP 36 phagocytes were the cell type that displayed differential gene expression. These phagocytes were 37 both able to sample C. albicans and able to discriminate between strains. In particular, strain 38 ATCC 18804 upregulated fungal specific pro-inflammatory genes in CD11c + phagocytes 39 pertaining to innate and adaptive immune responses. Interestingly, PP CD11c + phagocytes 40 differentially expressed genes in response to C. albicans that were important in the protection of 41 the mucosal barrier. These results highlight that the mucosal barrier not only responds to C. 42 albicans, but also aids in the protection of the host. 43 Importance 44The specific gene expression changes within PPs that send the warning signals when 45 encountering fungi, and how PPs can discriminate between innocuous S. cerevisiae or different 46 strains of C. albicans during early stages of sampling, have not been elucidated. Here we show 47 that within the first 24 hours of sampling, CD11c + phagocytes were not only important in 48 sampling, but they were the cell type that exhibited clear differential gene expression. These 49 differentially expressed genes play important dual roles in inflammation, chemotaxis, and fungal 50 specific recognition, as well as maintaining homeostasis and protection of the mucosal barrier. 51Using nanostring technology, we were also able to demonstrate that PPs can distinguish between 52 different strains of C. albicans and can "set off the alarms" when necessary. 53 54

show abstract

Molecular cloning and biophysical characterization of CXCL3 chemokine

Cited by 20 publications

References 37 publications

Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury

Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury

circMET promotes NSCLC cell proliferation, metastasis, and immune evasion by regulating the miR-145-5p/CXCL3 axis

Setting off the Alarms:Candida albicansElicits Pro-Inflammatory Differential Gene Expression in Intestinal Peyer’s Patches

Contact Info

Product

Resources

About