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Study · Animal study (in vivo) · mouse · 2020

13 results

Melanocortin therapy ameliorates podocytopathy and proteinuria in experimental focal segmental glomerulosclerosis involving a podocyte specific non-MC1R-mediated melanocortinergic signaling.

Qiao Y, Wang P, Chang M, Chen B, Ge Y, Malhotra DK, Dworkin LD, Gong R

Clinical science (London, England : 1979)1 Apr 2020Cited by 16 (Europe PMC)

PMID32167144 (opens in a new tab)PMCIDPMC9870294 (opens in a new tab)DOI10.1042/cs20200016 (opens in a new tab)PepBankPUB-32167144
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Summary

The clinical effectiveness of adrenocorticotropin in inducing remission of steroid-resistant nephrotic syndrome points to a steroidogenic-independent anti-proteinuric activity of melanocortins. However, which melanocortin receptors (MCR) convey this beneficial effect and if systemic or podocyte-specific mechanisms are involved remain uncertain. In vivo, wild-type (WT) mice developed heavy proteinuria and kidney dysfunction following Adriamycin insult, concomitant with focal segmental glomerulosclerosis (FSGS) and podocytopathy, marked by loss of podocin and synaptopodin, podocytopenia and extensive foot process effacement on electron microscopy. All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist. Surprisingly, MC1R deficiency in MC1R-null mice barely affected the severity of Adriamycin-elicited injury. Moreover, the beneficial effect of NDP-MSH was completely preserved in MC1R-null mice, suggesting that MC1R is likely non-essential for the protective action. A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility. Consistent with in vivo findings, the podoprotective activity of NDP-MSH was fully preserved in MC1R-null podocytes. Mechanistically, MC1R expression was predominantly distributed to glomerular endothelial cells in glomeruli but negligibly noted in podocytes in vivo and in vitro, suggesting that MC1R signaling is unlikely involved in direct podocyte protection. Ergo, melanocortin therapy protects against podocyte injury and ameliorates proteinuria and glomerulopathy in experimental FSGS, at least in part, via a podocyte-specific non-MC1R-mediated melanocortinergic signaling.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study13

13 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced FSGS, NDP-MSH attenuated heavy proteinuria.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced protein loss in the urine.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseProteinuria after Adriamycin
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    heavy proteinuria and kidney dysfunction
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced FSGS, NDP-MSH attenuated kidney dysfunction.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced kidney dysfunction.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseKidney dysfunction after Adriamycin
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    heavy proteinuria and kidney dysfunction
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced injury, NDP-MSH attenuated focal segmental glomerulosclerosis and podocytopathy.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced scarring in the kidney filter and damage to its podocyte cells.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseFocal segmental glomerulosclerosis and podocytopathy
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    concomitant with focal segmental glomerulosclerosis (FSGS) and podocytopathy
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced injury, NDP-MSH attenuated the loss of podocin and synaptopodin.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced the loss of two podocyte marker proteins.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseLoss of podocin and synaptopodin
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    loss of podocin and synaptopodin
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced injury, NDP-MSH attenuated podocytopenia.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced the loss of podocyte cells.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreasePodocytopenia
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    podocytopenia
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In wild-type mice with Adriamycin-induced injury, NDP-MSH attenuated extensive foot process effacement seen on electron microscopy.

    In plain wordsIn mice with kidney injury from Adriamycin, NDP-MSH reduced flattening of the podocyte foot processes.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseFoot process effacement
    Study

    Mousen: not reported in source

    Adriamycin-induced FSGS in wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    All these pathologic findings were prominently attenuated by NDP-MSH, a potent non-steroidogenic pan-MCR agonist.
    1 context sentence
    Summary · context
    extensive foot process effacement on electron microscopy.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In MC1R-null mice with Adriamycin injury, the beneficial effect of NDP-MSH was completely preserved, so MC1R is likely non-essential for the protection.

    In plain wordsIn mice lacking the MC1R receptor, NDP-MSH still protected the kidney, so this receptor is probably not needed for the protection.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseNDP-MSH protection in MC1R-null mice
    Study

    Mousen: not reported in source

    Adriamycin injury in MC1R-null mice
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, the beneficial effect of NDP-MSH was completely preserved in MC1R-null mice, suggesting that MC1R is likely non-essential for the protective action.
  8. 08LabIn vitro (cells)Efficacy outcome

    In primary mouse podocytes treated with Adriamycin, NDP-MSH mitigated apoptosis.

    In plain wordsIn lab-grown mouse podocytes damaged by Adriamycin, NDP-MSH reduced cell death.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreasePodocyte apoptosis in primary podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility.
  9. 09LabIn vitro (cells)Efficacy outcome

    In primary mouse podocytes treated with Adriamycin, NDP-MSH mitigated the loss of podocyte markers.

    In plain wordsIn lab-grown mouse podocytes damaged by Adriamycin, NDP-MSH reduced the loss of podocyte marker proteins.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseLoss of podocyte markers in primary podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility.
  10. 10LabIn vitro (cells)Efficacy outcome

    In primary mouse podocytes treated with Adriamycin, NDP-MSH mitigated de novo expression of the podocyte injury marker desmin.

    In plain wordsIn lab-grown mouse podocytes damaged by Adriamycin, NDP-MSH reduced a new injury-marker protein, desmin.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseDesmin expression in primary podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility.
  11. 11LabIn vitro (cells)Efficacy outcome

    In primary mouse podocytes treated with Adriamycin, NDP-MSH mitigated actin cytoskeleton derangement.

    In plain wordsIn lab-grown mouse podocytes damaged by Adriamycin, NDP-MSH reduced damage to the cell skeleton.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseActin cytoskeleton derangement in primary podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility.
  12. 12LabIn vitro (cells)Efficacy outcome

    In primary mouse podocytes treated with Adriamycin, NDP-MSH mitigated podocyte hypermotility.

    In plain wordsIn lab-grown mouse podocytes damaged by Adriamycin, NDP-MSH reduced excess cell movement.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreasePodocyte hypermotility in primary podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from wild-type mice
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A direct podocyte effect seems to contribute to the beneficial effect of NDP-MSH, because Adriamycin-inflicted cytopathic signs in primary podocytes prepared from WT mice were all mitigated by NDP-MSH, including apoptosis, loss of podocyte markers, de novo expression of the podocyte injury marker desmin, actin cytoskeleton derangement and podocyte hypermotility.
  13. 13LabIn vitro (cells)Mechanism

    In primary podocytes from MC1R-null mice, the podoprotective activity of NDP-MSH was fully preserved.

    In plain wordsIn lab-grown podocytes from mice lacking MC1R, NDP-MSH still protected the cells.

    Peptide
    Melanotan I (afamelanotide)
    Outcome
    DecreaseNDP-MSH podoprotection in MC1R-null podocytes
    Study

    Mousen: not reported in source

    Primary podocytes from MC1R-null mice
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistent with in vivo findings, the podoprotective activity of NDP-MSH was fully preserved in MC1R-null podocytes.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

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