MANF is widely expressed in mammalian tissues and differently regulated after ischemic and epileptic insults in rodent brain

Lindholm, Päivi; Peränen, Johan; Andressoo, Jaan‐Olle; Kalkkinen, Nisse; Kokaia, Zaal; Lindvall, Olle; Timmusk, Tõnis; Saarma, Märt

doi:10.1016/j.mcn.2008.07.016

Cited by 158 publications

(206 citation statements)

References 43 publications

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“…Consistently with the roles as extracellular NTFs, CDNF and MANF are secreted from transiently transfected cells (Lindholm et al, 2007(Lindholm et al, , 2008Palgi et al, 2009). Also the secretion of endogenous MANF has been demonstrated in vitro (Apostolou et al, 2008).…”

Section: Cdnf and Manf Ligandssupporting

confidence: 60%

“…Differently from human CDNF, mouse CDNF, or human and mouse MANF do not have potential N-or O-linked glycosylation sites. In contrast to the original report (Petrova et al, 2003), secreted glycosylated MANF has not been detected in later studies (Apostolou et al, 2008;Lindholm et al, 2008). Both CDNF and MANF are highly soluble and monomeric at neutral pH 7 (Lindholm et al, 2007;Mizobuchi et al, 2007).…”

Section: Cdnf and Manf Ligandsmentioning

confidence: 64%

“…Cerebral dopamine neurotrophic factor (CDNF; official name by HUGO gene nomenclature committee; previous name conserved dopamine NTF) and mesencephalic astrocyte-derived neurotrophic factor (MANF) form a novel evolutionary conserved protein family showing neurotrophic activities (Petrova et al, 2003;Lindholm et al, 2007Lindholm et al, , 2008Airavaara et al, 2009;Palgi et al, 2009;Voutilainen et al, 2009).…”

Section: Cdnf and Manf Ligandsmentioning

confidence: 99%

“…In support to that MANF protein added to the culture medium of cardiac myocytes prevented cell death induced by simulated ischemia in vitro . Manf was transiently upregulated in adult rat brain after status epilepticus (SE) and global forebrain ischemia in vivo (Lindholm et al, 2008), suggesting that MANF may regulate neuronal survival and synaptic plasticity in the cortex and hippocampus.…”

Section: Cdnf and Manf Activities In Vivomentioning

confidence: 99%

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Novel CDNF/MANF family of neurotrophic factors

Lindholm

Saarma

2010

Developmental Neurobiology

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Current therapeutic interventions for neurodegenerative diseases alleviate only disease symptoms, while treatments that could stop or reverse actual degenerative processes are not available. Parkinson's disease (PD) is a movement disorder with characteristic degeneration of dopaminergic neurons in the midbrain. Few neurotrophic factors (NTFs) that promote survival, maintenance, and differentiation of affected brain neurons are considered as potential therapeutic agents for the treatment of neurodegenerative diseases. Thus, it is important to search and study new NTFs that could also be used in therapy. In this review, we discuss novel evolutionary conserved family of NTFs consisting of two members in the vertebrates, cerebral dopamine neurotrophic factor (CDNF) and mesencephalic astrocyte-derived neurotrophic factor (MANF). Invertebrates, including Drosophila and Caenorhabditis have a single protein homologous to vertebrate CDNF/ MANF. Characteristic feature of these proteins is eight structurally conserved cysteine residues, which determine the protein fold. The crystal structure analysis revealed that CDNF and MANF consist of two domains; an amino-terminal saposin-like domain that may interact with lipids or membranes, and a presumably unfolded carboxy-terminal domain that may protect cells against endoplasmic reticulum stress. CDNF and MANF protect midbrain dopaminergic neurons and restore motor function in 6-hydroxydopamine rat model of PD in vivo. In line, Drosophila MANF is needed for the maintenance of dopaminergic neurites and dopamine levels in the fly, suggesting that the function of CDNF/MANF proteins is evolutionary conserved. Future studies will reveal the receptors and mode of action of these novel factors, which are potential therapeutic proteins for the treatment of PD. ' 2010 Wiley Periodicals, Inc. Develop Neurobiol 70: 360-371, 2010

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Section: Cdnf and Manf Ligandssupporting

confidence: 60%

Section: Cdnf and Manf Ligandsmentioning

confidence: 64%

Section: Cdnf and Manf Ligandsmentioning

confidence: 99%

Section: Cdnf and Manf Activities In Vivomentioning

confidence: 99%

See 2 more Smart Citations

Novel CDNF/MANF family of neurotrophic factors

Lindholm

Saarma

2010

Developmental Neurobiology

Self Cite

165

136

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“…Polymorphisms in CDNF have recently been linked to an early-onset form of PD [116]. Like CDNF, MANF is expressed in the rodent nigrostriatal system during the early postnatal period, as well as in the adult [117]. The Drosophila homologue of MANF, DmMANF, is essential for the maintenance and function of dopaminergic neurones [118].…”

Section: Effects Of Manf and Cdnf In Vitromentioning

confidence: 99%

Neurotrophic factors for the treatment of Parkinson's disease

Sullivan

Toulouse

2011

Cytokine & Growth Factor Reviews

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MANF attenuates neuronal apoptosis and promotes behavioral recovery via Akt/MDM‐2/p53 pathway after traumatic spinal cord injury in rats

Gao

Fan³

et al. 2018

BioFactors

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The aim of this study was to investigate the potential effect and mechanism of action of MANF in attenuating neuronal apoptosis following t-SCI. A clip compressive model was used to induce a crush injury of the spinal cord in a total of 230 rats. The Basso, Beattie, and Bresnahan (BBB) score, spinal cord water content, and blood spinal cord barrier (BSCB) permeability were evaluated. The expression levels of MANF and its downstream proteins were examined by western blotting. Immunofluorescence staining of MANF, NeuN, GFAP, Iba-1, cleaved caspase-3, and TUNEL staining were also performed. Cells were counted in six randomly selected fields in the gray matter regions of the sections from two spinal cord sites (2 mm rostral and caudal to the epicenter of the injury) per sample. A cell-based mechanical injury model was also conducted using SH-SY5Y cells. Cell apoptosis and viability were assessed by flow cytometry, an MTT assay, and trypan blue staining. Subcellular structures were observed by transmission electron microscopy. MANF was mainly expressed in neurons. The expression levels of MANF, and its downstream target, p-Akt, were gradually increased and after t-SCI. Treatment with MANF increased Bcl-2 and decreased Bax and CC-3 levels; these effects were reversed on treatment with MK2206. The BBB score, spinal cord water content, and BSCB destruction were also ameliorated by MANF treatment. MANF decreases neuronal apoptosis and improves neurological function through Akt/MDM-2/p53 pathway after t-SCI. Therefore, MANF might be a potential treatment for patients with t-SCI.© 2018 BioFactors, 2018.

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MANF is widely expressed in mammalian tissues and differently regulated after ischemic and epileptic insults in rodent brain

Cited by 158 publications

References 43 publications

Novel CDNF/MANF family of neurotrophic factors

Novel CDNF/MANF family of neurotrophic factors

Neurotrophic factors for the treatment of Parkinson's disease

MANF attenuates neuronal apoptosis and promotes behavioral recovery via Akt/MDM‐2/p53 pathway after traumatic spinal cord injury in rats

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