Kinin B1 receptor deficiency attenuates cisplatin-induced acute kidney injury by modulating immune cell migration

Estrela, Gabriel R.; Wasinski, Frederick; Almeida, Danilo Cândido de; Amano, Mariane Tami; Castoldi, Ângela; Dias, Carolina; Malheiros, Denise Maria Avancini Costa; Almeida, Sandro Soares de; Paredes‐Gamero, Edgar Julian; Pesquero, João Bosco; Barros, Carlos Castilho; Câmara, Niels Olsen Saraiva; Araújo, Ronaldo Carvalho

doi:10.1007/s00109-013-1116-z

Cited by 20 publications

(24 citation statements)

References 33 publications

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“…In fact, local IL-10 affects host immune response in many levels, including decrease in CD8 + T-cell-mediated tumor lysis, down regulation of major histocompatibility complex (MHC) class II and co-stimulatory molecules in dendritic cells 38 39 . Moreover, the kinin B1 receptor has been already associated with the migration of immune cells to injured tissues 40 . In our study, we observed that lungs from WT animals presented lower number of vessels compared to B1 receptor deficient mice.…”

Section: Discussionmentioning

confidence: 99%

Host kinin B1 receptor plays a protective role against melanoma progression

Maria

Dillenburg-Pilla

Reis

et al. 2016

Sci Rep

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Melanoma is a very aggressive tumor that arises from melanocytes. Late stage and widely spread diseases do not respond to standard therapeutic approaches. The kallikrein-kinin system (KKS) participates in biological processes such as vasodilatation, pain and inflammatory response. However, the role of KKS in tumor formation and progression is not completely understood. The role of the host kinin B1 receptor in melanoma development was evaluated using a syngeneic melanoma model. Primary tumors and metastasis were respectively induced by injecting B16F10 melanoma cells, which are derived from C57BL/6 mice, subcutaneously or in the tail vein in wild type C57BL/6 and B1 receptor knockout mice (B1−/−). Tumors developed in B1−/− mice presented unfavorable prognostic factors such as increased incidence of ulceration, higher levels of IL-10, higher activation of proliferative pathways such as ERK1/2 and Akt, and increased mitotic index. Furthermore, in the metastasis model, B1−/− mice developed larger metastatic colonies in the lung and lower CD8+immune effector cells when compared with WT animals. Altogether, our results provide evidences that B1−/− animals developed primary tumors with multiple features associated with poor prognosis and unfavorable metastatic onset, indicating that the B1 receptor may contribute to improve the host response against melanoma progression.

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Section: Discussionmentioning

confidence: 99%

Host kinin B1 receptor plays a protective role against melanoma progression

Maria

Dillenburg-Pilla

Reis

et al. 2016

Sci Rep

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“…Blockade of macrophage infiltration promotes a functional and histological renal protection, indicating a pathogenic role of macrophages [55–57] . Although no study has been conducted to identify the macrophage polarization in CN, several studies have indicated that macrophage infiltration is closely related to the pro-inflammatory cytokine release in the CN [58,59] . Therefore, it is presumable that these macrophages are M1 phenotype.…”

Section: Macrophage Polarization In Other Kidney Diseasesmentioning

confidence: 99%

Macrophage polarization in kidney diseases

2015

Macrophage

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Macrophage accumulation associates closely with the degree of renal structural injury and renal dysfunction in human kidney diseases. Depletion of macrophages reduces while adoptive transfer of macrophages worsens inflammation in animal models of the renal injury. However, emerging evidence support that macrophage polarization plays a critical role in the progression of a number of kidney diseases including obstructive nephropathy, ischemia-reperfusion injury, glomerulonephritis, diabetic nephropathy, and other kidney diseases. In this mini-review, we briefly summarize the macrophage infiltration and polarization in these inflammatory and fibrotic kidney diseases, discussing the results mostly from studies in animal models. In view of the critical role of macrophage in the progression of these diseases, manipulating macrophage phenotype may be a potential effective strategy to treat various kidney diseases.

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“…Multiple pathways and molecules are involved in cisplatin-induced nephrotoxicity and apoptosis is observed after cisplatin administration [ 31 , 32 ]. Apoptosis may occur in cisplatin treatment by activation of apoptotic pathways, such as intrinsic mitochondrial pathway and extrinsic pathway activated by death receptors [ 1 , 33 , 34 ]. TNFR-2 mediates apoptosis in cisplatin-induced injury and is one of the death receptors of the extrinsic pathway [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…TNFR-2 mediates apoptosis in cisplatin-induced injury and is one of the death receptors of the extrinsic pathway [ 35 ]. Moreover, the Bax/Bcl-2 ratio can be used to determine the intrinsic pathway of apoptosis [ 33 , 34 ]. Cisplatin treatment induced upregulation of TNFR- 2 and Bax/Bcl-2 ratio, while PPAR-α knockout mice are protected against this upregulation.…”

Section: Discussionmentioning

confidence: 99%

PPAR-α Deletion Attenuates Cisplatin Nephrotoxicity by Modulating Renal Organic Transporters MATE-1 and OCT-2

Freitas-Lima

Budu

Arruda

et al. 2020

IJMS

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Cisplatin is a chemotherapy drug widely used in the treatment of solid tumors. However, nephrotoxicity has been reported in about one-third of patients undergoing cisplatin therapy. Proximal tubules are the main target of cisplatin toxicity and cellular uptake; elimination of this drug can modulate renal damage. Organic transporters play an important role in the transport of cisplatin into the kidney and organic cations transporter 2 (OCT-2) has been shown to be one of the most important transporters to play this role. On the other hand, multidrug and toxin extrusion 1 (MATE-1) transporter is the main protein that mediates the extrusion of cisplatin into the urine. Cisplatin nephrotoxicity has been shown to be enhanced by increased OCT-2 and/or reduced MATE-1 activity. Peroxisome proliferator-activated receptor alpha (PPAR-α) is the transcription factor which controls lipid metabolism and glucose homeostasis; it is highly expressed in the kidneys and interacts with both MATE-1 and OCT-2. Considering the above, we treated wild-type and PPAR-α knockout mice with cisplatin in order to evaluate the severity of nephrotoxicity. Cisplatin induced renal dysfunction, renal inflammation, apoptosis and tubular injury in wild-type mice, whereas PPAR-α deletion protected against these alterations. Moreover, we observed that cisplatin induced down-regulation of organic transporters MATE-1 and OCT-2 and that PPAR-α deletion restored the expression of these transporters. In addition, PPAR-α knockout mice at basal state showed increased MATE-1 expression and reduced OCT-2 levels. Here, we show for the first time that PPAR-α deletion protects against cisplatin nephrotoxicity and that this protection is via modulation of the organic transporters MATE-1 and OCT-2.

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Kinin B1 receptor deficiency attenuates cisplatin-induced acute kidney injury by modulating immune cell migration

Cited by 20 publications

References 33 publications

Host kinin B1 receptor plays a protective role against melanoma progression

Host kinin B1 receptor plays a protective role against melanoma progression

Macrophage polarization in kidney diseases

PPAR-α Deletion Attenuates Cisplatin Nephrotoxicity by Modulating Renal Organic Transporters MATE-1 and OCT-2

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