Deep Wounds, Fast Defence: How Shark Skin Starts Healing Within Hours

A small shark living in cold Atlantic waters may hold valuable clues about how vertebrate skin protects itself after injury. In the study 'Wound Healing in Atlantic Spiny Dogfish Sharks,' published in Scientific Reports, researchers Etty Bachar-Wikstrom, Anthony Anselmo, Aaron R. Thorner, Inga Sidor, Lisa Abbo and Jakob D. Wikstrom found that Atlantic spiny dogfish can cover a full-thickness skin wound with a new epithelial layer within one day, even though deeper tissue repair continues for weeks.

The findings challenge the idea that healing must be slow in cold-water animals, whose metabolism and cellular activity are usually reduced by low temperatures. They also show that a wound can regain its protective surface well before the skin underneath has rebuilt its original structure.

Twenty sharks and 120 wounds revealed the pace of repair

The exploratory laboratory study involved 20 wild-caught female Atlantic spiny dogfish, scientifically known as Squalus acanthias. The animals were kept in flowing natural seawater at 14°C after being collected by commercial fishers near Chatham, Massachusetts.

Researchers created six standardized wounds on each shark using a four-millimetre biopsy punch, producing 120 wounds across the study group. These injuries passed through the full thickness of the skin, allowing the team to examine more than surface closure. Healing wounds were collected on Days 1, 14 and 35 using a larger punch that included the original injury and nearby tissue.

Serial photographs tracked changes in visible wound area for 35 days. Tissue sections were stained to show general skin structure, collagen, mucus-producing cells and possible bacteria. Single-nucleus RNA sequencing offered a closer look at the types of cells present in intact and injured skin, giving researchers a way to follow immune, epithelial, vascular, stromal, pigment, muscle and neural populations during repair.

Healthy dogfish skin contained an epidermis, a collagen-rich dermis and backwards-pointing placoid scales called dermal denticles. Keratinocytes, pigment-producing melanocytes and mucus-secreting cells were found between these tooth-like structures, while a thin mucus layer covered the surface.

A protective skin layer formed before the wound looked healed

Every wound examined on Day 1 was already covered by a continuous layer of migrating keratinocytes. These cells moved across a very thin collagen layer directly above the exposed muscle, creating a new surface before organized granulation tissue had formed. The response happened so completely that the researchers could not calculate different percentages of reepithelialization among the samples.

Blood cells had collected within fibrin clots, smaller numbers of inflammatory cells were present, and the basement membrane that normally supports the epidermis had not yet formed beneath the new covering. Mucus-producing cells were already appearing near the edge of the developing epidermis, suggesting that restoration of chemical and microbial protection begins soon after physical closure. Gram staining found no bacteria in the examined tissue sections.

Day 14 brought a much thicker neoepidermis containing several organized cell layers, including a newly established basal keratinocyte layer. The basement membrane had started to return, collagen was forming underneath, and the fibrin clot had become more organized. Mild inflammation, fluid between cells and immune-cell movement through the healing epidermis remained visible. The wound was smaller from the outside, though it still appeared depressed and incomplete.

On Day 35, the surface was no longer depressed, and it resembled a scar rather than fully restored skin. The epidermis remained unusually thick, dense collagen and mature granulation tissue occupied the dermis, and inflammatory cells were still moving through the tissue. A few dying epithelial cells may have signalled the beginning of a reduction in epidermal overgrowth. Dermal denticles had not returned, showing that rapid coverage did not equal complete regeneration of the shark's specialized skin.

Shark skin launched an early immune response

RNA sequencing identified 24 cellular clusters in the skin. Epithelial cells were the most abundant population in intact samples, followed by collagen-producing cells and mucus-associated cells. T cells were more common than endothelial cells, while B cells, probable mast cells and two groups of unidentified leukocytes were also detected, supporting the idea that healthy shark skin maintains a substantial resident immune community.

Two melanocyte populations, skeletal muscle cells, neural cells, vascular cells and a small group carrying cartilage-related markers were identified. The high number of muscle cells probably reflected the depth of the biopsies rather than an unusual feature of the outer skin.

Immune-cell proportions changed sharply after injury: B cells, T cells and unidentified leukocytes increased by Day 1, then most moved back toward their original levels by Day 14. B-cell representation rose to roughly 4.5 times its baseline value, one unidentified leukocyte group increased more than twentyfold, and erythrocytes rose nearly fivefold because the biopsy caused bleeding. Sharks produce unusual antibodies, including the heavy-chain-only IgNAR, though the study could not establish which immunoglobulins these early B cells were making.

Macrophages were not identified, despite their central role in mammalian and bony-fish healing. They may have been missed because shark immune markers remain poorly defined, may have appeared outside the sampled periods or could be represented by cells that the researchers could not classify.

Structural recovery followed a mixed timetable: One fibroblast group expanded strongly by Day 14, matching the collagen deposition and scar formation seen under the microscope. Mucosal cells stayed below baseline, indicating that secretory functions recovered more slowly than surface coverage. Muscle-cell representation fell by more than half on Day 1 and showed little recovery by Day 14. Neural populations initially declined and then returned, raising the possibility that peripheral nerves regenerate relatively quickly. Most endothelial cells remained stable, while two less clearly identified vascular populations expanded during healing.

Fast closure offers clues, not a direct treatment for people

Re-epithelialization within 24 hours places the cold-water dogfish alongside warm-water zebrafish, which are known for rapid healing, and ahead of cold-water salmonids, which generally need around three days to cover comparable wounds. Such speed could help sharks limit infection, abrasion and osmotic disruption while constantly exposed to seawater. Early mucus formation and the immediate rise in immune cells may provide added protection while deeper tissue remains vulnerable.

The conclusions remain preliminary because RNA samples from multiple biopsies were pooled at each time point, preventing statistical comparisons between individual animals. The Day 35 sequencing sample failed quality checks; only fixed sampling days were examined, and the gap between Days 1 and 14 may have missed important cellular events. Wild-caught sharks could also have responded to captivity-related stress, while roughly half of spiny dogfish genes still lack functional annotation. Single-nucleus sequencing can miss cytoplasmic and low-abundance RNA, which may have hidden certain genes or cell populations.