Expression of the neurotrophin receptor TrkB in the mouse liver

García‐Suárez, Olivia; González-Martínez, T.; Pérez-Pérez, M.; Germanà, Antonino; Blanco-Gelaz, Miguel Ángel; Monjil, Diego F.; Ciriaco, E.; Silos-Santiago, I.; Vega, J.A.

doi:10.1007/s00429-006-0098-9

Cited by 17 publications

(9 citation statements)

References 38 publications

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“…This protein is expressed on the neuronal cell bodies, axons, and dendrites in many cerebral structures [24]. In embryogenesis, TrkB is present in the monocyte-dendric cell fraction when the innervation of a particular organ is formed [25]. BDNF binding to this receptor maintains the differentiation and survival of neurons.…”

Section: Efficiency Of Different Differentiation Inducersmentioning

confidence: 99%

In Vitro Neuronal Induction of Adipose-Derived Stem Cells and their Fate after Transplantation into Injured Mouse Brain

Pavlova

Lopatina²,

Ni³

et al. 2012

CMC

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The effect of substances known as inducers of neuronal differentiation on cultured human and mouse adipose-derived mesenchymal stem cells (ASCs) and their fate after transplantation into the injured and ischemic mouse brains were studied. ASCs were isolated from the human and mouse adipose tissue. Inducers of neuronal differentiation included β-mercaptoethanol, glial cell line-derived neurotrophic factor (GNDF), brain-derived neurotrophic factor (BDNF), retinoic acid (RA), 5-azacytidine, as well as their combinations. Three days after the induction, the phenotype of the induced cells was analyzed using immunocytochemistry and real-time PCR assay for differential expression of specific genes. The induction efficiency was evaluated by the increased transcription of neuronal differentiation markers: nestin, β-III-tubulin (Tub-B), microtubule-associated protein 2 (MAP2), and neuron-specific enolase (ENO2). The expression of marker genes was tested by immunocytochemical analysis. ASC cultivation in the medium with RA or BDNF in combination with 5- azacytidine for a week increased the mRNA and protein levels of nestin, Tub-B, and ENO2. The transplantation of induced mouse ASCs into the mouse brain increased the lifespan of the cells relative to control uninduced cells and promoted their migration from the transplantation site to the recipient cerebral parenchyma. The transplantation of the induced cells into the mouse brain pre-exposed to endothelin- 1 promoted a more active cell migration into the surrounding ischemic brain tissue. Thus, ASC exposure to RA or BDNF in combination with 5-azacytidine elevated the transcription of the neuronal differentiation markers and improved the viability and integration of ASCs grafted into the mouse brain.

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Section: Efficiency Of Different Differentiation Inducersmentioning

confidence: 99%

In Vitro Neuronal Induction of Adipose-Derived Stem Cells and their Fate after Transplantation into Injured Mouse Brain

Pavlova

Lopatina²,

Ni³

et al. 2012

CMC

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“…The pattern of BDNF and TrkB expression suggests neurotrophic support of the autonomic innervation of the liver. In adult mice, whereas BDNF mRNA is expressed in mouse hepatocytes (Lommatzsch et al 1999), TrkB is expressed by periductal nerve fibers innervating the liver (Garcia-Suarez et al 2006).…”

Section: Bdnfmentioning

confidence: 99%

Neurotrophins and the Regulation of Energy Balance and Body Weight

Rios

2014

Handbook of Experimental Pharmacology

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Complex interactions between the brain and peripheral tissues mediate the effective control of energy balance and body weight. Hypothalamic and hindbrain neural circuits integrate peripheral signals informing the nutritional status of the animal and in response regulate nutrient intake and energy utilization. Obesity and its many medical complications emerge from the dysregulation of energy homeostasis. Excessive weight gain might also arise from alterations in reward systems of the brain that drive consumption of calorie dense, palatable foods in the absence of an energy requirement. Several neurotrophins, most notably brain-derived neurotrophic factor, have been implicated in the molecular and cellular processes underlying body weight regulation. Here, we review investigations interrogating their roles in energy balance and reward centers of the brain impacting feeding behavior and energy expenditure.

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“…The patterns of BDNF and TRKB expression suggest neurotrophic support of the autonomic innervation of the liver. In adult mice, whereas Bdnf mRNA is expressed in mouse hepatocytes (Lommatzsch et al 1999), TRKB is expressed by periductal nerve fibers innervating the liver (Garcia-Suarez et al 2006). As liver and portal vein afferents serve as sensors for amino acids, glucose, insulin, and glucagon, their expression of TRKB could facilitate the transmission of metabolic signals to the brain.…”

Section: Introductionmentioning

confidence: 99%

Diminished diet-induced hyperglycemia and dyslipidemia and enhanced expression of PPARα and FGF21 in mice with hepatic ablation of brain-derived neurotropic factor

Teillon¹,

Calderón²,

Rios³

2010

Journal of Endocrinology

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Brain-derived neurotropic factor (BDNF) mediates many aspects of neuronal function, and plays a chief role in the central regulation of energy balance. In the periphery, it is expressed in organs involved in energy, lipid, and glucose homeostasis, including the liver, but its role there remains unclear. Here, we describe studies examining the effect of selectively depleting hepatic BDNF. Liver-specific mutant mice exhibited normal food intake and body weights when fed standard chow or high-fat diets (HFDs). However, whereas HFD intake induced mild hyperglycemia and hyperinsulinemia in wild-types (WTs), liver-specific BDNF mutants were protected from these effects. Serum levels of cholesterol and triglycerides were also elevated in HFD-fed WTs, but they were normal or slightly increased in BDNF mutants. Furthermore, whereas WTs fed HFD exhibited elevated levels of circulating alanine aminotransferase and aspartate aminotransferase, BDNF mutant males fed a similar diet had a normal content of both enzymes. Molecular analysis indicated that the livers of BDNF mutants fed HFD contained elevated levels of peroxisome proliferator-activated receptor a (Ppara or Ppara as listed in the MGI Database) and fibroblast growth factor 21 (Fgf21) transcripts compared with WTs. This is a notable finding as this pathway has anti-diabetic and lipid clearance effects. Accordingly, genes involved in lipid and glucose handling and targets of PPARa and FGF21 were upregulated in the BDNF mutant livers. The collective data indicate that hepatic BDNF might facilitate the emergence of insulin resistance, dyslipidemia, and liver disease following HFD challenge by suppressing PPARa and FGF21.

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Expression of the neurotrophin receptor TrkB in the mouse liver

Cited by 17 publications

References 38 publications

In Vitro Neuronal Induction of Adipose-Derived Stem Cells and their Fate after Transplantation into Injured Mouse Brain

In Vitro Neuronal Induction of Adipose-Derived Stem Cells and their Fate after Transplantation into Injured Mouse Brain

Neurotrophins and the Regulation of Energy Balance and Body Weight

Diminished diet-induced hyperglycemia and dyslipidemia and enhanced expression of PPARα and FGF21 in mice with hepatic ablation of brain-derived neurotropic factor

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