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Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue
Irvine KA, Sahbaie P, Ferguson AR, Clark JD (2020) Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue. Exp Neurol 333:113428. doi: 10.1016/j.expneurol.2020.113428
Objective: To confirm hypothesis that dysfunctional descending noradrenergic and serotonergic pain control circuits may contribute to the loss of diffuse noxious inhibitory control (DNIC), a critical endogenous pain control mechanism, weeks to months after traumatic brain injury (TBI).
Summary: Results suggest that TBI causes maladaptation of descending nociceptive signaling mechanisms and changes in the function of both adrenergic and serotonergic circuits. Such changes could predispose those with TBI to chronic pain.
Usage: Anti-DBH-SAP (5 μg/5 μl) was injected in the left ventricle. Lesion of the LC resulted in failure of DNIC, an effect that mimics what is observed behaviorally after chronic TBI.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats.
Boccia L, Le Foll C, Lutz TA (2020) Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats. FASEB J 34(11):15448-15461. doi: 10.1096/fj.202001456RRR
Objective: To assess the phenotype of amylin activated LPBN (lateral parabrachial nucleus) neurons, especially to confirm the CGRPergic phenotype and to uncover the specific role of NA (noradrenaline) signaling from the AP to the LPBN.
Summary: The present study confirmed the central role of the LPBN in propagating amylin’s and sCT’s hypophagic action, and particularly the importance of AP → LPBN NA signaling in the mediation of this process, through the activation of LPBN (CGRP and non-CGRP) neurons.
Usage: The neuronal pathways used to process the physiological response to amylin were investigated using 50-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the area postrema (AP) or 25 ng into the lateral parabrachial nucleus (Potes et al., 2010).
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Spinal microglia-neuron interactions in chronic pain.
Ho IHT, Chan MTV, Wu WKK, Liu X (2020) Spinal microglia-neuron interactions in chronic pain. J Leukoc Biol 108:1575-1592. doi: 10.1002/JLB.3MR0520-695R
Summary: Spinal microglial activation is initiated shortly and persisted for more than 3 mo after partial sciatic nerve ligation. Intrathecal injection of Mac1-SAP, a saporin-conjugated anti-CD11b antibody to deplete microglia, abolished cold and mechanical allodynia for 2–12 wk after injury,92 supporting the role of activated microglia for chronic pain maintenance.
Related Products: Mac-1-SAP rat (Cat. #IT-33)
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Molecular genetics of kappa opioids in pain and itch sensations
Tseng PY, Hoon MA (2020) Molecular genetics of kappa opioids in pain and itch sensations. Handb Exp Pharmacol . doi: 10.1007/164_2020_397
Summary: The authors review the functions of the kappa opioid receptor (KOR) and its endogenous agonists dynorphins in modulating itch and pain. Nppb-SAP ablation of neurons expressing the Natriuretic olypeptide B receptor greatly reduced itch responses evoked by histamine or by intrathecal administration of Nppb, suggesting that these neurons transmit itch signals from Nppb primary afferents.
Related Products: Nppb-SAP (Cat. #IT-69)
Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss
Tapa S, Wang L, Francis Stuart SD, Wang Z, Jiang Y, Habecker BA, Ripplinger CM (2020) Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss. Sci Rep 10:18801. doi: 10.1038/s41598-020-75903-y
Summary: The authors present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing Anti-DBH-SAP.
Usage: Either 5μL of 40 ng/μL Anti-DBH-SAP or Mouse IgG-SAP (control) was applied three times directly to the exposed apical/anterior surface of the heart.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Cellular uptake of vitamin B12: Role and fate of TCblR/CD320, the transcobalamin receptor.
Gick GG, Arora K, Sequeira JM, Nakayama Y, Lai SC, Quadros EV (2020) Cellular uptake of vitamin B12: Role and fate of TCblR/CD320, the transcobalamin receptor. Exp Cell Res 396(1):112256. doi: 10.1016/j.yexcr.2020.112256
Summary: The increased and sustained expression of TCblR in proliferating cells has been used to target toxins preferentially to cancer cells and can be potentially used for targeted delivery of other anti-cancer drugs. In 2010 the authors published a paper which evaluated the potential of using immunotoxins to eliminate cancer cells expressing TCblR the authors performed a series of in vitro experiments using their monoclonal antibody plus Mab-ZAP in varying concentrations. The results indicated that this is a viable therapeutic model that causes minimal peripheral damage.
Related Products: Mab-ZAP (Cat. #IT-04)
Dexmedetomidine alleviates lipopolysaccharide-induced acute kidney injury by inhibiting p75NTR-mediated oxidative stress and apoptosis
Wang Z, Wu J, Hu Z, Luo C, Wang P, Zhang Y, Li H (2020) Dexmedetomidine alleviates lipopolysaccharide-induced acute kidney injury by inhibiting p75NTR-mediated oxidative stress and apoptosis. Oxid Med Cell Longev 2020:5454210. doi: 10.1155/2020/5454210 PMID: 33194004
Objective: To study antioxidant effects and the mechanism of Dexmedetomidine (DEX) in an inflammatory proximal tubular epithelial cell model and lipopolysaccharide- (LPS-) induced AKI in mice.
Summary: DEX ameliorated AKI in mice with sepsis by partially reducing oxidative stress and apoptosis through regulation of p75NTR/p38MAPK/JNK signaling pathways.
Usage: Western blot (1:5000); AB-N01AP: NGFr (mu p75) Rabbit Polyclonal
Related Products: NGFr (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)
Sulfatase 1 mediates IL-10-induced dimethylarginine dimethylaminohydrolase-1 expression and antiproliferative effects in vascular smooth muscle cells of spontaneously hypertensive rats
Kim HY, Kim HS (2021) Sulfatase 1 mediates IL-10-induced dimethylarginine dimethylaminohydrolase-1 expression and antiproliferative effects in vascular smooth muscle cells of spontaneously hypertensive rats. Cytokine 137:155344. doi: 10.1016/j.cyto.2020.155344 PMID: 33128921
Objective: To examine the effects of exSulfs on IL-10-induced dimethylarginine dimethylaminohydrolase-1 (DDAH-1) expression, abrogation of Ang II-induced DDAH-1 downregulation, and inhibition of Ang II-induced proliferation of spontaneously hypertensive rats (SHRs) vascular smooth muscle cells (VSMC). IL-10-induced DDAH-1 expression and abrogation of Ang II-induced DDAH-1 downregulation were attenuated in Sulf1 siRNA-transfected SHRs VSMC.
Summary: Sulf1, and not Sulf2, mediates the IL-10-induced inhibition of Ang II-induced hypertensive effects in SHRs VSMC.
Usage: Western blot (1:800)
Related Products: Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)
Gli1+ mesenchymal stromal cells form a pathological niche to promote airway progenitor metaplasia in the fibrotic lung
Cassandras M, Wang C, Kathiriya J, Tsukui T, Matatia P, Matthay M, Wolters P, Molofsky A, Sheppard D, Chapman H, Peng T (2020) Gli1+ mesenchymal stromal cells form a pathological niche to promote airway progenitor metaplasia in the fibrotic lung. Nat Cell Biol 22(11):1295-1306. doi: 10.1038/s41556-020-00591-9 PMID: 33046884
Objective: To show that Gli1+ mesenchymal stromal cells (MSCs) promote metaplastic differentiation of airway progenitors into KRT5+ basal cells.
Summary: Gli1+ MSCs integrate hedgehog signaling as a rheostat to control BMP activation in the progenitor niche to determine regenerative outcome in fibrosis.
Usage: Histology and Immunofluorescence (1:200)
Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)
The EphA2 and cancer connection: potential for immune-based interventions
London M, Gallo E (2020) The EphA2 and cancer connection: potential for immune-based interventions. Mol Biol Rep 47(10):8037-8048. doi: 10.1007/s11033-020-05767-y
Summary: The authors review the most current mAb-based therapies against EphA2-expressing cancers currently in pre-clinical and/or clinical stages. They reference Sakamoto et al. who performed in vitro testing of two different EphA2 mAbs mixed with Mab-ZAP to discover their therapeutic potential against melanoma.
Related Products: Mab-ZAP (Cat. #IT-04)