Midkine is a potent regulator of the catecholamine biosynthesis pathway in mouse aorta

Ezquerra, Laura; Herradón, Gonzalo; Nguyen, Trang; Silos‐Santiago, Inmaculada; Deuel, Thomas F.

doi:10.1016/j.lfs.2006.03.013

Cited by 11 publications

(8 citation statements)

References 56 publications

(71 reference statements)

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“…Levels of the dopamine synthesizing enzyme tyrosine hydroxylase (TH) are decreased in the striatum of Mdk −/− mice as measured by immunohistochemistry, and expression of the Th gene is higher in aorta from Mdk −/− mice compared with wild type mice (Ezquerra et al , 2006, Prediger et al , 2011). This suggests that a deficiency in Mdk leads to dysregulation of the dopamine system.…”

Section: Resultsmentioning

confidence: 99%

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Lasek

2017

Genes Brain and Behavior

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Midkine (MDK) is a cytokine and neurotrophic factor that is more highly expressed in the brains of human alcoholics and in mice predisposed to drink large amounts of ethanol, suggesting that MDK may regulate ethanol consumption. Here we measured ethanol consumption in male and female Mdk knockout (−/−) mice using the two-bottle choice and the drinking in the dark (DID) tests. We found that Mdk −/− mice consumed significantly more ethanol than wild type controls in both tests. To determine if MDK acts in the ventral tegmental area (VTA) to regulate ethanol consumption, we delivered lentivirus expressing a Mdk shRNA into the VTA of male C57BL/6J mice to locally knockdown Mdk and performed the DID test. Mice expressing a Mdk shRNA in the VTA consumed more ethanol than mice expressing a control non-targeting shRNA, demonstrating that the VTA is one site in the brain through which MDK acts to regulate ethanol consumption. Since MDK also controls the expression of inflammatory cytokines in other organs, we examined gene expression of interleukin-1 beta (Il1b), tumor necrosis factor alpha (Tnf) and the chemokine (C-C motif) ligand 2 (Ccl2) in the VTA of Mdk −/− mice and in mice expressing Mdk shRNA in the VTA. Expression of Ccl2 was elevated in the VTA of Mdk −/− mice and in mice expressing Mdk shRNA in the VTA. These results demonstrate that MDK functions in the VTA to limit ethanol consumption and levels of CCL2, a chemokine known to increase ethanol consumption.

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Section: Resultsmentioning

confidence: 99%

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Lasek

2017

Genes Brain and Behavior

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“…This is especially significant because, in addition to elevated circulating MDK in the serum of adult HF patients, circulating MDK has also been correlated with kidney dysfunction [ 34 ]. In addition to this, MDK has been found to mediate renin-angiotensin signaling as well as norepinephrine synthesis [ 70 , 71 ]. Taken together, this data indicates that MDK plays a vital and complicated role in cardiac function and pathology.…”

Section: Mdk In Cardiac Pathologymentioning

confidence: 99%

Midkine’s Role in Cardiac Pathology

Woulfe

Sucharov

2017

JCDD

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Midkine (MDK) is a heparin-binding growth factor that is normally expressed in mid-gestational development mediating mesenchymal and epithelial interactions. As organisms age, expression of MDK diminishes; however, in adults, MDK expression is associated with acute and chronic pathologic conditions such as myocardial infarction and heart failure (HF). The role of MDK is not clear in cardiovascular disease and currently there is no consensus if it plays a beneficial or detrimental role in HF. The lack of clarity in the literature is exacerbated by differing roles that circulating and myocardial MDK play in signaling pathways in cardiomyocytes (some of which have yet to be elucidated). Of particular interest, serum MDK is elevated in adults with chronic heart failure and higher circulating MDK is associated with worse cardiac function. In addition, pediatric HF patients have higher levels of myocardial MDK. This review focuses on what is known about the effect of exogenous versus myocardial MDK in various cardiac disease models in an effort to better clarify the role of midkine in HF.

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“…The replacement targeting vector generated a PTN null allele (PTN 2-4neo) by deleting exons 2 to 4. MK-/-mice were generated as previously described by using a basic vector to target a part of exon 1, intron 1 and a part of exon 2 of MK (Ezquerra et al, 2005(Ezquerra et al, , 2006Nakamura et al, 1998). Male PTN-/-, MK-/-and WT mice on a 129/Ola x C57BL/6J background were used at 8-10 weeks of age (20-25 g).…”

Section: Ptn and Mk Genetically Deficient Micementioning

confidence: 99%

Differential phosphoproteome of the striatum from pleiotrophin knockout and midkine knockout mice treated with amphetamine: Correlations with amphetamine-induced neurotoxicity

et al. 2013

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Midkine is a potent regulator of the catecholamine biosynthesis pathway in mouse aorta

Cited by 11 publications

References 56 publications

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Midkine’s Role in Cardiac Pathology

Differential phosphoproteome of the striatum from pleiotrophin knockout and midkine knockout mice treated with amphetamine: Correlations with amphetamine-induced neurotoxicity

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